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BACKGROUND: In recent years, artificial intelligence has gradually emerged and has been applied in various fields such as spinal cord nerve injury and repair, which has a positive impact on clinical treatment. OBJECTIVE: To study the application progress of artificial intelligence in the diagnosis, treatment, and rehabilitation of spinal cord nerve injury and repair, clarify the research hotspots and shortcomings in this field, and provide suggestions for future research work. METHODS: Relevant literature on artificial intelligence in the field of spinal cord nerve injury and repair was retrieved on the Web of Science core collection database until 2023. CiteSpace 6.1.R6 and VOSviewer 1.6.19 software was used to perform general literature analysis, co-citation of literature, co-citation of journals, double image overlay of journals, keyword clustering, and other visual analysis on the literature data. RESULTS AND CONCLUSION: (1) A total of 1 713 articles were selected, and the annual publication volume in this field showed a fluctuating upward trend, with the United States taking the lead, and Kadone and Hideki being the authors with the highest publication volume. ARCH PHYS MED REHAB was the journal with the highest number of citations. (2) Keyword co-occurrence and cluster analysis showed that after removing keywords similar to the search terms, the main keywords were divided into three main clusters: Exoskeleton and exercise rehabilitation (the largest core hotspot); machine learning and neural plasticity; robotics and rehabilitation training. (3) Keyword burst analysis showed that deep learning and artificial intelligence had become burst terms in the past five years. (4) The results of in-depth analysis of co cited and highly cited literature showed that the hotspots of artificial intelligence in the field of spinal cord nerve injury and repair were mainly focused on powered exoskeletons, gaits, electrical nerve stimulation, intracortical brain-computer interface (IBCI), robots, and polymer biomaterials, and neural stem cell. (5) The research on artificial intelligence in the field of spinal cord nerve injury and repair has shown an upward trend in recent years. The focus of this field had gradually shifted from single treatment methods such as exoskeletons and electrical stimulation to intelligent, precise, and personalized directions. (6) There were some limitations in this field, such as the consequences of missing or imbalanced data, low data accuracy and reproducibility, and ethical issues (such as privacy, research transparency, and clinical reliability). Future research should address the issue of data collection, requiring large sample, high-quality clinical datasets to establish effective artificial intelligence models. At the same time, the research on genomics and other mechanisms in this field is very weak. In the future, various machine learning technologies such as brain chips can be used, and gene editing therapy, single-cell spatial transcriptome and other methods can be used to study the basic mechanisms of regeneration-related gene upregulation and axon growth structural protein production. [ABSTRACT FROM AUTHOR]

BACKGROUND: Electrical stimulation is an effective treatment plan for peripheral nerve injuries, but different frequencies of electrical stimulation have different mechanisms and applications for promoting peripheral nerve recovery. OBJECTIVE: To systematically sort out and summarize the roles and applications of different frequencies of electrical stimulation in the treatment of peripheral nerve injuries, and to deeply analyze the advantages and disadvantages of various methods in order to find the most beneficial treatment strategy for patients’ nerve recovery METHODS: Computer-based searches were conducted in the China National Knowledge Infrastructure (CNKI) and PubMed databases from the inception of the databases to May 2024. The search terms included “peripheral nerve injury, electrical stimulation, low frequency electrical stimulation, medium frequency electrical stimulation, high frequency electrical stimulation, TENS, interfering electricity, short wave, ultrashort wave, frequency” in both English and Chinese. Ultimately, 74 relevant documents were included for analysis. RESULTS AND CONCLUSION: Peripheral nerve injury, a common clinical disease, can cause sensory and motor dysfunction in patients. Low-frequency electrical stimulation can promote cell proliferation and accelerate the expression of nerve growth factor within the cell after electrical stimulation, promote macrophage recruitment and infiltration, accelerate the clearance of myelin debris, and promote myelin regeneration of damaged axons. Medium-frequency electrical stimulation can act on deeper tissues and is better for relieving neuropathic pain. High-frequency electrical stimulation can promote the proliferation of Schwann cells and macrophages, inhibit inflammatory factors, and rapidly recruit cells to the site of nerve injury, accelerating the speed of nerve repair. Different frequencies of electrical stimulation have their own advantages in promoting the recovery of peripheral nerve injuries, but there are still some issues, such as differences in the site of electrical stimulation and the treatment plans for various disease types. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of exosomes secreted by bone marrow mesenchymal stem cells (BMSCs) on the proliferation, migration, brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) secretion of Schwann cells. Methods Exosomes secreted by BMSCs were extracted from bilateral femoral bone marrow of 3-week-old SD rats, and Schwann cells were extracted from bilateral sciatic nerves of 3-day-old SD rats. Schwann cells were divided into the control group and BMSCs group. Cells in the control group were cultured with Schwann cell medium, and cells in the BMSCs group were cultured with Schwann cell medium containing 100 µg/mL BMSCs exosomes. When Schwann cells were cultured for 24, 48 and 72 h, the proliferation of Schwann cells in the two groups was observed by CCK-8 (expressed by OD value). When Schwann cells were cultured for 24 and 48 h, the migration abilities of Schwann cells in the two groups were observed by Scratch test (expressed by migration relative area ratio). When Schwann cells of the two groups were cultured for 72 h, the secretion capacities of BDNF and VEGF were observed by ELISA method (represented by the content of BDNF and VEGF in the cell supernatant). Results The OD values of Schwann cells cultured for 24, 48 and 72 h were 1. 06 ± 0. 04, 1. 22 ± 0. 06 and 1. 42 ± 0. 08, respectively, in the control group, versus 1. 46 ± 0. 11, 1. 70 ± 0. 10 and 1. 94 ± 0. 19, respectively, in the BMSCs group, with statistically significant difference (all P<0. 05). The relative area ratios of Schwann cells in the control group were 26. 43% ± 4. 75% and 45. 44% ± 3. 41% at 24 and 48 h, respectively, and those in the BMSCs group were 46. 29% ± 3. 88% and 65. 04% ± 2. 85%, respectively, with statistically significant difference (all P<0. 05). The content of BDNF in the supernatant of Schwann cells cultured for 72 h in the control group was (72. 48 ± 7. 25) pg/mL, and that in the supernatant of Schwann cells in the BMSCs group was (109. 70 ± 6. 38) pg/mL, with statistically significant difference (P<0. 05). Conclusion Exosomes secreted by BMSCs can promote the proliferation, migration and the secretion of BDNF and VEGF of Schwann cells, thus contributing to nerve regeneration. [ABSTRACT FROM AUTHOR]

Spinal cord injury has the characteristics of high mortality and disability rates, and the treatment of spinal cord injury has been a worldwide problem. With the deepening of spinal cord injury research and the advancement of treatment methods, the survival rate of patients has improved, but the clinical efficacy is still not ideal. New research has found that the immune response is involved in the entire process of pathological changes and regeneration and repair after spinal cord injury. Among them, the complement system plays an important role in the occurrence and development of spinal cord injury. This article mainly reviews the role of the complement system in secondary spinal cord injury and regeneration and repair after spinal cord injury, including the doubleedged sword effect of the complement system, the impact of the complement system on axonal regeneration and synaptic maintenance, and possible signaling pathways, with a view to improving the treatment of spinal cord injury, providing new treatment ideas.

BACKGROUND: Although nerve conduits provide an effective treatment approach for nerve repair, traditional nerve conduits merely serve as mechanical channels in the repair process. The therapeutic effect still needs to be improved. Carbon nanomaterials have good physicochemical properties and hold great potential in fields such as electrochemistry and tissue engineering. Nerve conduits loaded with carbon nanomaterials, after appropriate functional modifications, are expected to further enhance the quality of nerve repair. OBJECTIVE: To review the recent research progress of carbon nanomaterial-loaded nerve conduits/scaffolds for peripheral nerve repair. METHODS: PubMed, Web of Science, China National Knowledge Infrastructure (CNKI), and Wanfang databases were searched for the literature on the application of carbon nanomaterial catheters in peripheral nerve regeneration. English keywords were “carbon nanomaterials, carbon-based nanomaterials, nerve conduit, nerve guidance conduit, scaffold, nerve regeneration, peripheral nerve repair, peripheral nerve injury” and Chinese keywords were “carbon nanomaterials, carbon materials, graphene, carbon nanotubes, nerve conduits, nerve scaffolds, nerve repair, nerve regeneration, peripheral nerve injury”. Finally, 69 articles were selected for this review. RESULTS AND CONCLUSION: (1) Carbon nanomaterials primarily restore damaged neural bioelectric signal conduction by activating calcium ion channels and inducing intracellular calcium activity. The application of various nerve conduit design strategies has improved the effectiveness of nerve repair. (2) Successful intraneural vascularization is the prerequisite for repairing peripheral nerve injuries. Reactive oxygen species and reactive nitrogen species generated by carbon nanomaterials trigger subsequent signaling pathways that promote intraneural vascularization. (3) The ratio of M1 to M2 macrophages affects the repair of peripheral nerve injuries. Carbon nanomaterials promote the polarization of macrophages into the M2 phenotype, thereby exerting their anti-inflammatory and regenerative effects. (4) Some carbon nanomaterials may induce excessive generation of reactive oxygen species intracellularly, potentially exhibiting cytotoxicity detrimental to nerve repair. However, appropriate functional modifications can improve the adverse effects caused by carbon nanomaterials. (5) Although carbon nanomaterials can restore the microenvironment of peripheral nerve injuries and play a positive role in promoting peripheral nerve regeneration, their inherent cytotoxicity and unclear in vivo degradation pathways still pose challenges for clinical application. However, by employing methods such as functional modification, it is possible to enhance the biocompatibility of carbon nanomaterials. Modified carbon nanomaterials have promising prospects in the field of neural tissue engineering. [ABSTRACT FROM AUTHOR]

BACKGROUND: Previous studies had shown that hair follicle epidermal neural crest stem cells have the great potential in facilitating peripheral nerve rehabilitation, but the role in regulating inflammation after facial nerve injury had rarely been reported. OBJECTIVE: To investigate whether epidermal neural crest stem cells can modify the expression of pro-inflammatory factor tumor necrosis factor α and anti-inflammatory factor interleukin-4 during facial nerve regeneration to promote the functional and morphological recovery of the facial nerve. METHODS: Epidermal neural crest stem cells were extracted from one 4-day-old SD rat, cultured and identified. Fifty-four adult SD rats were used to construct the bridge model of facial nerve trunk defect with the autologous venous catheter. Models were randomly and equally divided into the normal saline group, Dulbecco's modified eagle medium group and epidermal neural crest stem cell group. Tumor necrosis factor α and interleukin-4 expression levels were detected at postoperative 4 to 14 days using western blotting, immunohistochemistry, and immunofluorescence. The facial nerve function of rats was scored 12 weeks after the operation and the morphology of the facial nerve was observed by hematoxylin-eosin staining. RESULTS AND CONCLUSION: (1) Double positive expression of Nestin and p75NTR could be observed in epidermal neural crest stem cells and the cell purity was over 90%. (2) Compared with the other two groups, tumor necrosis factor α expression in the epidermal neural crest stem cell group turned weaker 7 days after surgery (P < 0.05), and interleukin-4 expression in the epidermal neural crest stem cell group was enhanced on postoperative 3, 7 and 14 days, respectively (P < 0.05). (3) The recovery score of facial nerve function in the epidermal neural crest stem cell group was significantly better than that in the other two groups (P < 0.05). (4) There were abundant nutrient vessels and regenerative axons in the graft segment. Compared with the other two groups, the arrangement of nerve fibers was more orderly and the wrapped myelin sheath was thicker in the graft and distal segment in the epidermal neural crest stem cell group. (5) The data inferred that epidermal neural crest stem cells regulate the local expression of tumor necrosis factor α and interleukin-4 at the early stage of facial nerve injury, inhibit the local inflammatory reaction, and improve facial nerve function and morphology of the regenerated nerve. [ABSTRACT FROM AUTHOR]

Fracture is the most common large-organ injury in humans. It takes several months or even longer from the onset to the completion of bone reconstruction. In severe cases, delayed healing or even bone discontinuity can occur. The current treatment of fractures mainly pursues the completion of clinical healing and bone healing, and the healing process is divided into three stages: early, intermediate and late. Various factors affect the speed of the healing process, among which signaling pathways and cytokines play an important role in fracture healing, so understanding the important role of signaling pathways and cytokines is important for treating fractures and promoting fracture healing. Recent studies have shown that the Notch signaling pathway can affect cell proliferation and differentiation, inflammatory response, bone reconstruction, angiogenesis and nerve regeneration during fracture healing, and its changes are also closely related to mechanical stimulation and other factors. Therefore, this paper reviews the research progress in the role of Notch signaling pathway in various aspects of fracture healing from the perspectives of cell proliferation and differentiation, inflammatory response, bone reconstruction, angiogenesis, nerve regeneration and mechanical stimulation, and provides new research directions and therapeutic strategies for fracture healing treatment.

BACKGROUND: Non-invasive treatment of spinal cord injury needs to be developed urgently. Nanomaterials have obvious advantages, which can deliver drugs and improve the therapeutic effect. OBJECTIVE: To fabricate sustained-release nanospheres containing neurotrophin-3 and ganglioside GD1a by poly(lactic-co-glycolic acid) and investigate their effects on the repair of spinal cord injury in rats. METHODS: Poly(lactic-co-glycolic acid) nanospheres encapsulated with neurotrophin-3 and ganglioside GD1a were prepared using oil-water emulsion volatile organic solvent method. The sustained release properties of microspheres were tested. Sixty female adult SD rats were randomly divided into five groups with 12 rats in each group. In the sham operation group, the lamina was opened and sutured directly. In the spinal cord injury group, a spinal cord T9 impingement injury model was established. In the neurotrophin group, the nanosphere suspension of slow-release neurotrophin-3 was injected into the injured area of spinal cord T9. In the ganglioside GD1a group, the sustained-release ganglioside GD1a nanosphere suspension was injected into the spinal cord T9 injury area. The experimental group was injected with nanosphere suspension of sustained-release neurotrophin-3 and ganglioside GD1a in the injured area of spinal cord T9. Open field test and BBB scoring were conducted weekly after operation. The sections were taken 4 and 8 weeks after surgery for morphological observation. RESULTS AND CONCLUSION: (1) After soaking in PBS for 14 days in vitro, the sustained-release nanospheres could continuously release neurotrophin-3 and ganglioside GD1a. (2) At 7 and 8 weeks after surgery, compared with the spinal cord injury group, the BBB score and the total open field distance of the rats increased in the neurotrophin group and the experimental group (P < 0.05). The results of Nissl staining showed that at 4 and 8 weeks after surgery, the number of motor neurons increased in the anterior horn of caudal gray matter in the experimental group compared with the spinal cord injury group (P < 0.05). At 8 weeks after surgery, the number of motor neurons increased in the anterior horn of caudal gray matter in the neurotrophin group compared with the spinal cord injury group (P < 0.05). The results of immunofluorescence staining showed that compared with the spinal cord injury group, the neurotrophin group at 8 weeks and the experimental group at 4 and 8 weeks had increased spinal white matter ventral nerve fibers (P < 0.05); the expression of myelin basic protein on the ventral side of the spinal cord white matter increased at 4 and 8 weeks in the ganglioside GD1a and experimental groups (P < 0.05); the expression of myelin basic protein in the neurotrophin group increased at 8 weeks after operation (P < 0.05); the descending propriospinal tract increased in the neurotrophin group and the experimental group at 8 weeks (P < 0.05). (3) The results showed that neurotrophin-3 microspheres alone or in combination with ganglioside GD1a microspheres could promote the survival of motor neurons and nerve fibers around the spinal cord injury site and improve the motor function of the hind limbs of rats. [ABSTRACT FROM AUTHOR]

In the treatment of neurological diseases, neuroregeneration is a contentious and challenging issue. Our understanding of the mechanisms related to neuroregeneration in neuromyelitis optica spectrum disorders (NMOSDs) is currently restricted and there lack of effective treatment to promote neuroregeneration and repair. To enhance the knowledge of neuroregeneration in NMOSDs, this article will concentrate on the challenge, current research progress, and future research directions. It will provide suggestions for investigating potential treatments for neuroregeneration in this condition.

BACKGROUND: Neural stem cells have the effect of repairing, replacing damaged nerve cells, stimulating neurogenesis, rebuilding cell circuits, inhibiting apoptosis, and have shown a good therapeutic effect in the study of Alzheimer’s disease. Traditional Chinese medicine also has significant efficacy on regulating the proliferation and differentiation of neural stem cells and improving nerve cell viability and cell survival. OBJECTIVE: To review the mechanism of traditional Chinese medicine regulating neural stem cells in the treatment of Alzheimer’s disease, so as to provide a reference for the research and treatment of new drugs for Alzheimer’s disease. METHODS: The articles on Wanfang, CNKI, PubMed, Web of Science and other databases about neural stem cell regulated by traditional Chinese medicine in the treatment of Alzheimer’s disease from 2010 to 2022 were searched, with “neural stem cells, traditional Chinese medicine, Alzheimer’s disease” as the key words in Chinese and English. The outdated and repetitive viewpoints were excluded, and the retrieved articles were analyzed and sorted out, and a total of 121 articles were included for analysis. RESULTS AND CONCLUSION: (1) The definition and pathogenesis of neural stem cells and Alzheimer’s disease were sorted out. (2) The mechanism of action of traditional Chinese medicine in regulating neural stem cells in the treatment of Alzheimer’s disease was summarized, mainly including promoting the proliferation of neural stem cells, improving the microenvironment in the brain, inhibiting the apoptosis of nerve cells, inducing neural stem cell differentiation into neurons, improving neuroinflammation, and regulating vascular nerve units. (3) Through the existing research, the relevant factors and signaling pathways of traditional Chinese medicine to regulate neural stem cells in the treatment of Alzheimer’s disease were summarized, such as Nestin protein, microtubuleassociated protein, cerebrogenic neurotrophic factor, vascular endothelial growth factor and Notch signal pathway, P13k/Akt signaling pathway, brain-derived neurotrophic factor/TrkB signaling pathway, and Wnt/β-catenin signaling pathway. It may provide a relevant reference for the future research on new drugs for Alzheimer’s disease and new clinical treatment methods. [ABSTRACT FROM AUTHOR]

Objective To investigate the protective effect and mechanism of platelet-rich plasma (PRP) on facial nerve injury. Methods A total of 100 rats were used in the experiment, in which 10 rats were used for PRP preparation, 10 rats were set as the control group (group A), and the other 80 rats were used to construct the crush model of facial nerve injury. After the surgery, the 80 rats were randomly divided into 2 groups with 40 rats in each. Group B was given continuous injection of normal saline for 1 week, which was the natural recovery group; group C was given continuous injection of PRP in the local operative area for 1 week, which was the PRP treatment group. The facial nerve function of the rats in each group was observed immediately, 1 week, 2 weeks and 3 weeks after PRP or saline intervention by behavioral and neuroelectrophysiological observation. The facial nerve was observed by electron microscopy and the glial cells were observed by hematoxylin-eosin (HE) staining. The platelet-activating growth factor (PAF), nuclear factor-κB (NF-κB) and tumor necrosis factor-α (TNF-α), brain-derived neurotrophic factor (BDNF), neurotrophic factor -4 (NT-4) in the facial nerve nucleus were detected by polymerase chain reaction (PCR). Results Behavioral evaluation: on the first day after intervention, the injury sides of group B and group C presented complete facial paralysis. Three weeks after intervention, the facial paralysis score of group C was significantly higher than that of group B, and the difference was statistically significant (P< 0.05). Neuroelectrophysiological assessment: compared with group A, the latency of facial nerve complex muscle action potentials (CMAPs) in groups B and groups C was significantly prolonged and the amplitude of CMAPs was decreased on day 1 after intervention. Three weeks after intervention, the incubation period of group C was significantly shortened and the amplitude of the wave was significantly increased. More Schwann nuclei and regenerated myelin sheath were observed in group C facial nerves under electron microscope. The facial nerve nucleus mass staining showed that the normal facial nerve motor neuron cell body was a typical multipolar motor neuron, distributed around with the glial cells. The mRNA levels of PAF, NF-κB, TNF-α, BDNF and NT-4 were all increased after injury, and the differences were all statistically significant (P <0.01). PRP reduced mRNA levels of these factors. Conclusions PRP has a protective effect on traumatic facial nerve injury, and the possible mechanisms include inhibiting the activation of PAF and the production of inflammatory mediators and upregating neurotrophic factors. [ABSTRACT FROM AUTHOR]

Schwann cells (SCs) have a strong plasticity. After peripheral nerve injury, Schwann cells dedifferentiate into repair phenotype and dominate the repair process. C-Jun N-terminal kinase, mitogen activated protein kinase(MAPK) and other signaling pathways and transcriptional regulators are involved in regulating Schwann cell-mediated repair process. This review discusses the main signaling pathways and transcriptional regulators of Schwann cell promoting peripheral nerve regeneration.

BACKGROUND: Due to the weak regeneration ability after spinal cord injury, it is still a difficult medical problem to repair the damaged spinal cord tissue and normalize its function. The rapid development of biological tissue materials and its wide application in medicine provide new therapeutic ideas and methods for spinal cord injury repair. OBJECTIVE: To summarize the research situation of biomaterial scaffolds on nerve tissue regeneration and repair after spinal cord injury, and forecast its development trend, so as to explore the methods of spinal cord injury repair and summarize experience. METHODS: The articles published from January 2011 to January 2021 were retrieved using the advanced retrieval function of PubMed database. The search terms were “spinal cord injury; biomaterials; nerve regeneration; material”. By using the advanced retrieval functions of CNKI, Wanfang, VIP and other databases, relevant articles published from January 2011 to January 2021 were searched, and the search terms were “spinal cord injury; biomaterials; scaffolds”. RESULTS AND CONCLUSION: With further development of the combination of bioengineering research and medicine, biomaterial scaffolds have been widely used in the study of spinal cord injury repair, and the histocompatibility and degradation of biomaterials have been improved. There are many kinds of biomaterials, each of which has its own advantages and disadvantages. It is better to prepare composite scaffolds loaded with seed cells, cytokines or drugs for nerve regeneration. However, how to select the composite scaffold material combination, how to select the seed cells, cytokines or drugs, so as to make the biomaterial scaffold combined with seed cells, cytokines or drugs become the best combination value of in-depth research. In conclusion, biomaterial repair of spinal cord injury is a new idea and may become a breakthrough point to promote the repair of spinal cord injury. [ABSTRACT FROM AUTHOR]

BACKGROUND: Glial fibrillary acidic protein is an intermediate filament overexpression protein, which is the most commonly used specific marker protein for astrocytes. Traditional Chinese medicine has a long history of treating spinal cord injury. Numerous studies have shown that acupuncture at Du Meridian and Stomach Meridian of Foot-Yangming has a certain therapeutic effect on nerve regeneration and repair after spinal cord injury. OBJECTIVE: To observe the changes in the expression of glial fibrillary acidic protein in the injured part of spinal cord injury rats after electroacupuncture stimulation, and to further investigate the effect of electroacupuncture on nerve regeneration in rats with spinal cord injury. METHODS: A total of 120 Sprague-Dawley rats were randomly divided into 5 groups (n=24 per groups): a Du Meridian electroacupuncture group, a Stomach Meridian of Foot-Yangming electroacupuncture group, a mixed electroacupuncture group, a model control group, and a sham operation group. T10 spinal cord hemisection models were prepared in all the groups except for the sham operation group. After modeling, each group was randomly subdivided into four subgroups (n=6 per group): a 3-day group, a 7-day group, a 14-day group, and a 21-day group. The sham operation group and the model control group were not given an intervention, and the three electroacupuncture groups were given a corresponding electroacupuncture intervention. Immunohistochemical staining was used to detect the expression of glial fibrillary acidic protein positive cells in the injured area. PCR and western blot were used to detect the mRNA and protein expression of glial fibrillary acidic protein. RESULTS AND CONCLUSION: Compared with the sham operation group, the expression of glial fibrillary acidic protein after injury was increased first and then decreased significantly in the model control group (P < 0.05). Compared with the model control group, the expression of glial fibrillary acidic protein was significantly reduced in the Du Meridian electroacupuncture group and the Stomach Meridian of Foot-Yangming electroacupuncture group (P < 0.05). The expression of glial fibrillary acidic protein in the mixed electroacupuncture group was lower than that in the Du Meridian electroacupuncture group and the Stomach Meridian of Foot-Yangming electroacupuncture group, but there was no significant difference (P > 0.05). To conclude, electroacupuncture stimulation can reduce the expression of glial fibrillary acidic protein and astrocytes in the injured area, thereby inhibiting the formation of glial scars. [ABSTRACT FROM AUTHOR]

BACKGROUND: The transient receptor potential vanilloid 4 (TRPV4) agonist GSK1016790A can activate TRPV4 protein and induce Ca2+ influx in a short time, while its expression remains unchanged. However, during culture, the decreased expression of TRPV4 on HeLa cell membrane surface was induced by GSK1016790A. Whether the phenomenon had an effect on neural regeneration is still not clear. OBJECTIVE: To explore the effect of TRPV4 agonist GSK1016790A on axonal regeneration in different periods. METHODS: The dorsal root ganglion cells of ICR mouse at 6-8 weeks were treated by collagenase and trypsin for cell culture. In the 2-hour group, the agonist GSK1016790A was added at the initial stage of culture and the cells were treated for 2 hours and the culture was continued for 3 days. The 3-day group was treated with the agonist GSK1016790A for 3 days. The blank control group did not undergo any treatment. The TRPV4 protein expression and axon regeneration related protein expression were examined by western blot assay. TUJ1 and TRPV4 immunofluorescence staining was performed simultaneously. Number of axon branches, length of axon regeneration, and number of cell survival were counted. RESULTS AND CONCLUSION: (1) Compared with the blank control group, there was no significant difference in TRPV4 protein changes after GSK101 stimulated nerve cells for 2 hours (P > 0.05); while the expression of TRPV4 decreased significantly after nerve cells were stimulated for 3 days (P < 0.05). (2) Compared with the blank control group, after GSK1016790A stimulated nerve cells for 2 hours, there was no significant difference in the number of axon branches and axon length (P > 0.05); after stimulating nerve cells for 3 days, the number of axon bifurcations and axon length were increased significantly (P < 0.05). (3) Compared with the blank control group, there was no significant change in cell survival rate after GSK1016790A stimulated nerve cells for 2 hours or 3 days. (4) Compared with the blank control group, after GSK1016790A stimulated nerve cells for 3 days, the expression of PTEN decreased (P < 0.05), and the regeneration of nerve axons was significant. This process may be mediated by inhibiting the expression of PTEN protein. [ABSTRACT FROM AUTHOR]

BACKGROUND: As a class of nano-scaled biomaterials, nanoparticles have exhibited outstanding performances in promoting neural stem cells proliferation and differentiation, delivering therapeutic molecules and drugs, and scavenging excessive radical oxygen species. OBJECTIVE: To summarize the properties of nanoparticles for the treatment of ischemic stroke, and to analyze their therapeutic effects and related treatment mechanism on the pathological process of ischemic stroke. METHODS: The author searched the relevant articles collected by PubMed, Wanfang, and China National Knowledge Infrastructure database from January 2000 to December 2020. The key words were “ischemic stroke, nanomaterials, nanoparticles, nanozyme” in English, and “ischemic stroke or cerebral infarction, nanoparticles, nanozyme” in Chinese. Based on the inclusion and exclusion criteria, 79 articles were finally selected for review. RESULTS AND CONCLUSION: Nanoparticles have made great progress in the treatment of ischemic stroke. A large number of studies have shown that (1) nanoparticles can be used as a drug delivery system to deliver neuroprotective drugs and molecules and to achieve targeted drug delivery across the bloodbrain barrier. (2) Nanoparticles can promote brain tissue regeneration through their inherent anti-oxidation properties. (3) Nanoparticle combined with stem cell therapy can improve the efficacy of endogenous neurogenesis and exogenous stem cell transplantation. However, a very little proportion of studies have focused on this field, and meanwhile lacking a systematic design standard and optimal formulation of nanoparticles for ischemic stroke treatment. In the future, it is necessary to further explore the disease mechanism of ischemic stroke and fully understand the interaction between nanoparticles and biological systems, thereby designing a brain-targeted nanoparticle therapy system to promote its clinical application. [ABSTRACT FROM AUTHOR]

BACKGROUND: Growth-associated protein 43, as a membrane-like phosphoprotein, is a marker protein of neuronal regeneration plasticity and participates in the key process of axonal regeneration and the connection of various stages. It is of great significance for central nerve regeneration. OBJECTIVE: To investigate the mechanism of nerve regeneration and recovery after spinal cord injury by observing the interaction of neurite outgrowth inhibitor A (Nogo-A)/neurite growth inhibitor receptor (NgR) signaling pathway and nerve growth factor (NGF)/tyrosine kinase (TrkA) signaling pathway on the expression of growth-associated protein 43. METHODS: A total of 120 Sprague-Dawley rats were randomly divided into 5 groups: NgR blocking group, TrkA blocking group, double blocking agent group, injury control group, and sham surgery group. Rats in the sham surgery group underwent laminectomy (without injury to the spinal cord); and spinal cord injury rat models were established in the other groups. Immediately after successful modeling, rats in the NgR blocking group were injected with 25 μL of NEP1-40, a NgR blocker, and 25 μL of normal saline in the injured segment. Rats in the TrkA blocking group were injected with 25 μL of K252a, a TrkA blocker, and 25 μL of normal saline. Rats in the double blocking agent group were injected with 25 μL of NEP1-40 and 25 μL of K252a. Rats in the injury control group and the sham surgery group were injected with 50 μL of normal saline. On the 3rd, 7th, 14th, and 21st days after the intervention, the mRNA and protein expression of growthassociated protein 43 in rat spinal cord tissue were detected by immunohistochemistry, PCR, and western blot. RESULTS AND CONCLUSION: The results of immunohistochemistry, PCR, and western blot showed that the mRNA and protein expression of growth-associated protein 43 in the NgR blocking group, the TrkA blocking group, the double blocking agent group and the injury control group was higher than that in the sham surgery group. The expression of growth-associated protein 43 in the NgR blocking group and the double blocking agent group was higher than that in the injury control group, and there was a significant difference on the 7th and 14th days (P < 0.05 or P < 0.01). The mRNA and protein expression of growth-associated protein 43 in the TrkA blocking group was lower than that in the injury control group, and the difference was significant on the 7th and 14th days (P < 0.05 or P < 0.01). To conclude, the results from the NgR blocking group proves that the Nogo-A/NgR signaling pathway can significantly increase the expression of growth-associated protein 43 and promote the regeneration of nerve axons. The results from the TrkA blocking group proves that the NGF/TrkA signaling pathway can reduce the expression of growth-associated protein 43 and inhibit the regeneration of nerve axons. The results from the double blocking agent group shows that the interaction of the Nogo-A/NgR signaling pathway and the NGF/TrkA signaling pathway can promote the expression of growth-associated protein 43. [ABSTRACT FROM AUTHOR]

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Objective To construct a nerve catheter by crosslinking hepatocyte growth factor（HGF） into collagen catheter and observe its therapeutic effect in the rat model with facial nerve injury. Methods 12 male rats were randomly divided into HGF group and PBS group. Facial nerve injury model was established by removing a 10 mm long segment of the buccal branch nerve. Functional assessment and morphological evaluation were carried out 8 weeks after operation. Results Significant vibrissae movement improvement was observed in HGF group as compared with controls in PBS group（P < 0. 01）. The nerve conduction velocity measured in the HGF group was significantly faster than those in PBS group（P < 0. 01）. The myelination thickness and nerve fibers were significantly higher in HGF group, in contrast to that in PBS group. Conclusion Local crosslink of HGF in collagen tube as nerve conduit could accelerate functional recovery after transection of facial nerve. [ABSTRACT FROM AUTHOR]

BACKGROUND: Clinical manifestations of spinal cord injury are related to the severity and location of injury. Although the research on spinal cord injury has lasted for many years, there is still no effective treatment to restore the function of injured spinal cord. OBJECTIVE: To review the characteristics of astrocytes, the activation of reactive astrocytes in recent years and the related therapeutic strategies. METHODS: In PubMed database, the key words of “spinal cord injury, astrocyte” were searched. The key words of “spinal cord injury, astrocyte” were searched in Wanfang and CNKI. The retrieval time limit was from January 2010 to October 2020. According to the inclusion and exclusion criteria, articles unrelated to the research purpose, long-standing and repetitive articles were excluded, and 61 articles meeting the criteria were included for review. RESULTS AND CONCLUSION: The physiological functions of astrocytes are diverse and are very important for maintaining the stability of the central nervous system. Astrocytes can also be activated into reactive astrocytes after spinal cord injury, which will have beneficial or adverse effects on the nervous system. Treatment of spinal cord injury with astrocytes can effectively improve neurological function, reduce inflammatory reaction after spinal cord injury, and promote axon growth and remyelination. The activation types and mechanisms of reactive astrocytes need to be further explored, and the safety and cost issues of related treatment strategies need to be further solved. Therefore, it is necessary to explore the mechanism of astrocytes in spinal cord injury. [ABSTRACT FROM AUTHOR]

The corneal nerve originates from the trigeminal nerve, which mainly innervates the corneal sensation. Therefore, corneal nerve injury and decrease of corneal sensation occur when the trigeminal nerve is damaged. Neurotrophic keratopathy (NK) is a disease related with alterations in corneal nerves, leading to corneal epithelial defects, ulcer and perforation. However, mild NK is mostly manifested as a slight decrease in corneal sensation and instability of the tear film, so it is quite insidious in clinical practice. At the same time, the clinical treatment methods for promoting corneal reinnervation and restoring corneal sensation are usually relatively simple. Currently, medical treatment, non-surgical interventions and surgical interventions are the treatments for NK thus promoting corneal nerve and sensation recovery. In addition to maintaining the stability of the ocular surface, the main purpose of medical treatment is anti-infection and anti-inflammation, and to prevent further damage to the cornea. Novel biological agents are also under clinical trials such as platelet-rich plasma, autologous serum and recombinant human nerve growth factor. Nonsurgical intervention which mainly includes therapeutic contact lenses, medical tape and botulinum toxin injections aims to reduce corneal exposure and protect the cornea. With regard to surgical interventions, in addition to the conventional procedures aimed at repairing corneal defects and reducing the exposed area, there is also a new procedure called corneal nerve transplantation, which is aimed at improving corneal sensation and corneal innervation. Corneal nerve transplantation is a new surgical method that is directly targeted at improving corneal sensation and innervation. It is an ideal surgical method for patients with loss of corneal subbasal nerve fibers due to trigeminal nerve injury. In conclusion, medical treatment, non-surgical intervention and surgical neurotization are not separated in clinical practice. This article summarizes the progress of the application of the above three types of treatments in order to provide a reference for the future clinical selection of appropriate treatment modalities and comprehensive reconstruction of corneal sensation according to the course and different severity of disease development. [ABSTRACT FROM AUTHOR]

To investigate the mechanism of MiRNA-125a-5p on inflammatory response, apoptosis and nerve regeneration after spinal cord injury (SCI). Methods: The SCI model of 6-week-old rats was established. 60 rats were randomly divided into control group (n=20), SCI group (n=20) and MiRNA-125a-5p group (n=20). Only laminectomy was performed in the control group, rats in SCI group were injected with the same amount of normal saline, and rats in MiRNA-125a-5p group were injected with MiRNA-125a-5pagomir. The relative RNA expression levels of MiRNA-125a-5p and nuclear factor kB (NF-kB) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The expressions of inflammatory factors interleukin-1 (IL-1), chemokine receptor-4 (CXCR-4)and monocyte chemokine-1 (MCP-1) were detected by enzyme-linked immunosorbent assay (ELISA). The expressions of apoptosis protein and neuroregulatory factor protein were detected by Western blot. Basso Beattie Bresnahan (BBB) motor ability rating scale was used to evaluate the neuromotor function of rats. Results: Compared with the control group, the expression of MiRNA-125a-5p decreased and the expression of NF-kB increased in SCI group (P<0.05); Compared with SCI group, the expression of MiRNA-125a-5p increased and the expression of NF-kB decreased in MiRNA-125a-5p group (P<0.05). Compared with the control group, the levels of IL-1, CXCR-4and MCP-1 in SCI group were significantly higher (P<0.05). Compared with SCI group, the levels of IL-1, CXCR-4 and MCP-1 in MiR-NA-125a-5p group were significantly lower (P<0.05). Compared with the control group, the expressions of caspase-3, cleaved PARP andbcl-2 protein in SCI group were increased, and the expressions of NCAM1, NL1 and NRG1 protein were decreased (P<0.05); Compared with SCI group, the expression of caspase-3 and cleaved PARP protein in MiRNA-125a-5p group decreased, and the expression of bcl-2,NCAM1, NL1 and NRG1 protein increased (P<0.05). Compared with the control group, the neuromotor function score of SCI group decreased significantly after the 7th day (P<0.05); Compared with SCI group, the neuromotor function scores of rats in MiRNA-125a-5pgroup increased after the 7th day, and the difference was statistically significant (P<0.05). Conclusion:MiRNA-125a-5p inhibits NF-kB signaling pathway, reduces inflammatory response and apoptosis, promotes nerve regeneration and improves the recovery of neuromotor function in rats. [ABSTRACT FROM AUTHOR]

Objective: To describe the research progress of silk-based biomaterials in peripheral nerve repair and provide useful ideals to accelerate the regeneration of large-size peripheral nerve injury., Methods: The relative documents about silk-based biomaterials used in peripheral nerve regeneration were reviewed and the different strategies that could accelerate peripheral nerve regeneration through building bioactive microenvironment with silk fibroin were discussed., Results: Many silk fibroin tissue engineered nerve conduits have been developed to provide multiple biomimetic microstructures, and different microstructures have different mechanisms of promoting nerve repair. Biomimetic porous structures favor the nutrient exchange at wound sites and inhibit the invasion of scar tissue. The aligned structures can induce the directional growth of nerve tissue, while the multiple channels promote the axon elongation. When the fillers are introduced to the conduits, better growth, migration, and differentiation of nerve cells can be achieved. Besides biomimetic structures, different nerve growth factors and bioactive drugs can be loaded on silk carriers and released slowly at nerve wounds, providing suitable biochemical cues. Both the biomimetic structures and the loaded bioactive ingredients optimize the niches of peripheral nerves, resulting in quicker and better nerve repair. With silk biomaterials as a platform, fusing multiple ways to achieve the multidimensional regulation of nerve microenvironments is becoming a critical strategy in repairing large-size peripheral nerve injury., Conclusion: Silk-based biomaterials are useful platforms to achieve the design of biomimetic hierarchical microstructures and the co-loading of various bioactive ingredients. Silk fibroin nerve conduits provide suitable microenvironment to accelerate functional recovery of peripheral nerves. Different optimizing strategies are available for silk fibroin biomaterials to favor the nerve regeneration, which would satisfy the needs of various nerve tissue repair. Bioactive silk conduits have promising future in large-size peripheral nerve regeneration.

Objective·To investigate the effect of heat shock protein 70 (HSP70) on cryopreserved rat sciatic nerve cell activity and nerve regeneration after allotransplantation. Methods·Bilateral sciatic nerves of SD rats were placed in DMEM medium and pretreated with heat stress in vitro at 37 ℃, 42 ℃ and 45 ℃ for 1 h (37 ℃ group, 42 ℃ group and 45 ℃ group, respectively). A fresh nerve group was set up as the control (Con) group. The number of nerves in each group was 36. The expression of HSP70 in sciatic nerve was detected by Western blotting. The previously described nerves were stored in a cryopreservation solution with liquid nitrogen for 4 weeks. The expressions of major histocompatibility complex class Ⅰ (MHC-Ⅰ), MHC-Ⅱ, caspase-3 and caspase-9 were determined by Western blotting. The survival of sciatic nerve cells was detected by flow cytometry. The cryopreserved sciatic nerves were cultured at 37 ℃ with 5% CO2 for 7 d. The expressions of brain-derived neurotrophic factors (BDNF) and glial cell line-derived neurotrophic factors (GDNF) were detected by Western blotting. The cryopreserved sciatic nerves and the fresh sciatic nerves of SD rats were employed to repair the 10-mm-defect of sciatic nerve in the corresponding Wistar rats in the 37 ℃-Allo group, 42 ℃-Allo group, 45 ℃-Allo group, Con-Allo group and Fresh-Allo group. Meanwhile, an isograft group was also established (Fresh-Iso group). Each group had six Wistar rats. After 20 weeks of transplantation, the compound muscle action potential (CMAP) and nerve conduction velocity (NCV) were detected using electrophysiology. Toluidine blue staining was performed to observe the number of regenerated myelinated nerve fibers. The ultrastructure of the regenerated nerves was visualized through a transmission electron microscope. Results·HSP70 expression level was higher in the 42 °C group than that in the 37 °C group, 45 °C group and Con group, respectively (all P<0.05). After 4 weeks of cryopreservation, the expressions of MHC-Ⅰ and MHC-Ⅱ in the 42 ℃ group were not statistically different from those in the 37 ℃ group, 45 ℃ group and Con group, respectively. The expression levels of caspase-3 and caspase-9 in the 42 °C group were lower than those in the 37 °C group, 45 °C group and Con group, respectively, and the survival rate of sciatic nerve cells was increased (all P<0.05). After 7 d of culture, the expressions of BDNF and GDNF in the 42 ℃ group were higher than those in the 37 ℃ group, 45 ℃ group and Con group (all P=0.000), respectively. After 20 weeks of the transplantation, CMAP, NCV, the number of myelinated nerve fibers and myelin sheath thickness in the 42 °C-Allo group were superior to those in the Cont-Allo group and Fresh-Allo group (all P=0.000). Conclusion·Highly expressed HSP70 can minimize cryopreservation injury in sciatic nerves of rats, improve nerve cell viability after preservation, and promote nerve regeneration after allotransplantation. [ABSTRACT FROM AUTHOR]

Objective This study investigated the effects of different implant surface properties on the biological behavior of Schwann cells. Methods Schwann cells (SCs) were cultured on three types of implant surfaces including smooth polished (SMO), sand-blasted, large grit, acid-etched (SLA), and chemically-modified SLA (modSLA). At different time points, the morphology and adhesion of SCs on the implant surfaces were observed by scanning electron microscope. Cell proliferation activity was detected by MTT method. The expression levels of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) were detected by enzyme-linked immunosorbent assay. Changes in the mRNA levels of NGF and BDNF were detected by real-time fluorescent quantitative polymerase chain reaction (PCR). Results SCs adhered, stretched, and proliferated well on the three types of implant surfaces. On the 3rd, 5th, and 7th days, the OD values of the SMO group were higher than those of the SLA group and the modSLA group, and the difference was statistically significant (P<0.05). On the 3rd day, the expression and mRNA levels of NGF and BDNF in the SLA group and the modSLA group were higher than those in the SMO group (P<0.05); in particular, the levels in the modSLA group were higher than those in the SLA group (P<0.05). Conclusion Different implant surface properties have different effects on the biological behavior of SCs. Proliferation of SCs is significantly promoted by smooth surface, while secretion and gene expression of neurotrophic factors are significantly promoted by modSLA surface at early stage. [ABSTRACT FROM AUTHOR]

BACKGROUND: The repair of peripheral nerve defects by nerve conduit bridging can provide a suitable microenvironment for nerve regeneration. On one hand, it can provide a unique channel for nerve regeneration, prevent the invasion of peripheral connective tissue and the formation of scars. On the other hand, it can maintain endogenous and exogenous neurotrophic factors, growth factors and other stimulants to promote axon growth. OBJECTIVE: To observe the therapeutic effect of chitosan/polyvinyl alcohol catheter injected with brain-derived neurotrophic factor sustained-release microspheres to bridge peripheral nerve defects. METHODS: Chitosan/polyvinyl alcohol nerve conduit was prepared by repeated freeze-thaw technique. The brain-derived neurotrophic factor microspheres were obtained by polymer-alloys combined with oil-oil emulsion/solvent evaporation method. A 15 mm sciatic nerve defect model was made in the right hindlimb of 60 adult male Sprague-Dawley rats. They were selected and randomly divided into four groups (n=15 per group): group A implanted with autogenous sciatic nerve; group B implanted with chitosan/polyvinyl alcohol nerve catheter, injected with normal saline; group C implanted with chitosan/polyvinyl alcohol nerve catheter, injected with brain-derived neurotrophic factor solution; group D implanted with chitosan/polyvinyl alcohol nerve catheter, injected with brain-derived neurotrophic factor sustained-release microspheres. General observation, histological inspection, and electrophysiological determination were performed at 4 months after the surgery. This study was approved by the Research Ethics Committee of the Second Hospital of Hebei Medical University. RESULTS AND CONCLUSION: (1) Gross anatomy showed that muscle atrophy in group A and group D was lighter than that in the other two groups. The grafts in four groups were all adhered to the peripheral tissues, and the nerve in the autotransplantation segment was strongly adhered to the peripheral tissues. In group D, the regenerated nerve had connected the distal and proximal nerves, and the regenerated nerve filled the conduit. (2) Electrophysiological examination showed that the latency of group D was shorter than that of groups B and C (P< 0.01), and the evoked potential and conduction velocity of group D were higher than that of groups B and C (P < 0.01). There was no significant difference between group D and group A (P > 0.05). (3) Histological observation showed that there were regenerated nerve fibers in groups B, C, and D. The diameter, number and thickness of myelin sheath of group D were larger than those of group B and group C (P < 0.01). There was no significant difference between group D and group A (P> 0.05). (4) The results showed that the injection of brain-derived neurotrophic factor microspheres into chitosan/PVA catheter had a long-term promoting effect on peripheral nerve regeneration. [ABSTRACT FROM AUTHOR]

BACKGROUND: Spinal cord injury often leads to patients’ permanent sensory, motor and autonomic dysfunction because of limited inherent regeneration capacity of the central nervous system. Spinal cord injury seriously affects patients’ quality of life but there is still no effective treatment for it. The existing studies suggest that mesenchymal stem cell secretome mediates the main therapeutic effect of cell transplantation and avoids problems such as cellular rejection, so it will become a powerful tool for the treatment of spinal cord injury. OBJECTIVE: To summarize the research progress of mesenchymal stem cell secretome in the treatment of spinal cord injury, and analyze the current problems and future development direction. METHODS: The PubMed database was retrieved with “spinal cord injury, secretome” as the keywords, and Chinese databases include CNKI and Wanfang were retrieved with “spinal cord injury, secretome” as the keywords in Chinese. We retrieved the articles published from January 2013 to January 2020 and excluded the articles that were irrelevant or repetitive. At last 71 articles that met the criteria were included for review. RESULTS AND CONCLUSION: The mesenchymal stem cell secretome is rich in extracellular vesicles and soluble molecules such as growth factors and neurotrophic factors, and it plays prominent place in reducing cell apoptosis, regulating immune response, inhibiting scar formation, promoting nerve regeneration and angiogenesis. Numerous studies have shown that the mesenchymal stem cell secretome can promote nerve regeneration and function recovery after spinal cord injury, and it avoids the disadvantages of cell transplantation. The mesenchymal stem cell secretome will become a reliable method to treat spinal cord injury in the future. [ABSTRACT FROM AUTHOR]

Stroke brings the pathological changes of brain tissues such as hematoma formation or ischemia and hypoxia, which leads to neuronal death and axon degeneration. Axon regeneration after its injury is mainly dependent on the surrounding microenvironment and the related proteins, including glial scar, myelin associated inhibitory factors, axon guidance molecules, and neurotrophic factors. All of them affect axon growth by regulating the morphology and orientation of growth cones, the synaptic stability, and the proliferation and differentiation of neural stem cells. This article summarizes the mechanism of acupuncture in regulating axon regeneration after stroke. Acupuncture inhibits glial scar formation, alleviates the inhibitory effects of its physical and chemical barriers on axon growth, reverses the inhibitory effects of myelin-related inhibitory factors on axon growth, and adjusts the level of axon guidance molecules to promote the proliferation and differentiation of neural stem cells and the regeneration of injured axons, and up-regulates neurotrophic factors. Eventually, post-stroke nerve injury can be ameliorated.

BACKGROUND: Platelet-rich plasma (PRP) contains growth factors that affect tendon, ligament, muscle and bone hesling. On this basis, researchers gradually realize that such molecules released after PRP activation can regulate the early inflammation of peripheral nerve injury, activate Schwann cells, promote the polarization of macrophages, and actively prevent the hyperplasia of collagen fibers, thus becoming the key drivers of nerve function recovery. OBJECTIVE: To evaluate the value of ultrasound-guided PRP injection in the repair of sciatic nerve crush injury. METHODS: Twenty-eight heslthy New Zealand white rabbits provided by the Beijing Longan Experimental Animal Breeding Center) were randomly divided into normal group, control group, single PRP group and multiple PRPs group. In the normal group, the right sciatic nerve was exposed and then sutured directly. In the control group, a compression injury model of the right sciatic nerve was established. In the single PRP group, autologous PRP was injected around the injured nerve under ultrasound guidance at 24 hours after modeling. In the multiple PRPs group, autologous PRP was injected around the injured nerve under ultrasound guidance at 24 hours after modeling, and then the PRP injection was performed once at the 3rd and 5th weeks after modeling. Histological and morphological observation of regenerated nerves, wet weight recovery and histological manifestations of the denervated muscle were evaluated at 12 weeks after modeling. The study protocol was approved by the Administrative Committee of Experimental Animals in PLA General Hospital with the approval No. 2015-x10-02. RE SUL TS AND CONCLUSION: The integral optical density values of NF-200 and S 100 staining, myelinated nerve fiber density, myelinated nerve fiber diameter and myelin sheath thickness were significantly increased in the single PRP and multiple PRPs groups compared with the control group (all P < 0.05), and the multiple PRPs group showed better outcomes than the single PRP group {all P < 0.05), but was still inferior to the normal group (all P < 0.05). Compared with the control group, wet weight and cross-sectional area of muscle fibers significantly increased in the single PRP group and multiple PRPs group (P < 0.05), and the multiple RPRs group showed better outcomes than the single PRP group, but was still inferior to the normal group (P < 0.05). To conclude, ultrasound-guided multi-frequency injection of autologous PRP has a good effect on the repair of sciatic nerve crush injury. [ABSTRACT FROM AUTHOR]

BACKGROUND: The mechanism of electroacupuncture on multi-acupoints in the treatment of peripheral facial paralysis is still unknown. Glial cell-derived neurotrophic factor (GDNF) is currently the most effective factor in promoting the survival of motoneurons in vitro, and the PI3K/AKT pathway plays an important role in protecting damaged motoneurons. There is yet no research on GDNF/PI3K/AKT pathway involved in electroacupuncture promoting facial nerve regeneration in rabbits. OBJECTIVE: To observe the effect of electroacupuncture on regeneration after peripheral facial nerve crush injury, and to explore the protective mechanism of electroacupuncture on facial motoneurons through the GDNF/PI3K/AKT signaling pathway. METHODS: Sixty-six adult healthy New Zealand white rabbits provided by the Animal Experimental Center of Southwest Medical University were randomly divided into a normal group and a model group. The facial nerves on the right side in the model group were subjected to a crush injury. Then the animal models were randomly divided into a model control group and an electroacupuncture group. Animals in the model control group recovered naturally, while those in the electroacupuncture group underwent electroacupuncture at Yifeng, Jiache, Sibai, Dicang, Yangbai, and Quanliao acupoints daily for 30 minutes. The improvement of facial paralysis symptoms in experimental animals were observed and scored. Tissue samples were directly taken form the normal group, and pons tissues with facial neurons were taken in the model group at 1, 4, 7, 14, and 28 days postoperatively. The morphologies of facial motoneurons and Nissl bodies were observed by hematoxylin-eosin staining and Nissl staining, respectively. Immunohistochemical techniques and western blot assay were used to detect the protein expression of GDNF, PI3K, AKT, and p-AKT in the facial motoneurons. The study protocol was approved by the Animal Ethics Committee of Southwest Medical University with approval No. 20170120001. RESULTS AND CONCLUSION: The symptoms of facial paralysis were that the animal’s mouth was drooped at the affected side, with lodging tentacles and the movement being weakened, and the eyelids that could not be lifted, which recovered faster and more completely in the electroacupuncture group than the model control group. The morphological changes of facial neurons and changes of Nissl bodies in the electroacupuncture group were lighter than those in the model control group. At each time point postoperatively, the stronger GDNF immune response could be seen in the electroacupuncture group, and the number of GDNF-positive cells was higher than that of the model control group except 1 day postoperatively (P < 0.001). The expressions of GDNF, PI3K, p-AKT proteins in the facial motoneurons were significantly increased in the electroacupuncture group compared with the model control group (P < 0.05; P < 0.01; P < 0.001). To conclude, electroacupuncture can effectively treat the peripheral facial paralysis caused by the crushed injury of facial nerve and promote the recovery of facial neurons. The up-regulation of GDNF expression in the facial motoneurons and the activation of PI3K/AKT signaling pathway may be the underlying protective mechanism of electroacupuncture. [ABSTRACT FROM AUTHOR]

Objective: To investigate the feasibility of selenium-methylselenocysteine (SMC) to promote peripheral nerve regeneration and its mechanism of action., Methods: Rat Schwann cells RSC96 cells were randomly divided into 5 groups, which were group A (without any treatment, control group), group B (adding 100 μmol/L H 2 O 2 ), group C (adding 100 μmol/L H 2 O 2 +100 μmol/L SMC), group D (adding 100 μmol/L H 2 O 2 +200 μmol/L SMC), group E (adding 100 μmol/L H 2 O 2 +400 μmol/L SMC); the effect of SMC on cell proliferation was detected by MTT method, and the level of oxidative stress was detected by immunofluorescence for free radicals [reactive oxygen species (ROS)] after determining the appropriate dose group. Thirty-six 4-week-old male Sprague Dawley rats were randomly divided into 3 groups, namely, the sham operation group (Sham group), the sciatic nerve injury group (PNI group), and the SMC treatment group (SMC group), with 12 rats in each group; the rats in the PNI group were fed with food and water normally after modelling operation, and the rats in the SMC group were added 0.75 mg/kg SMC to the drinking water every day. At 4 weeks after operation, the sciatic nerves of rats in each group were sampled for neuroelectrophysiological detection of highest potential of compound muscle action potential (CMAP). The levels of inflammatory factors [interleukin 17 (IL-17), IL-6, IL-10 and oxidative stress factors catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA)] were detected by ELISA assay. The luxol fast blue (LFB) staining was used to observe the myelin density, fluorescence intensity of glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) was observed by immunofluorescence staining, and myelin morphology was observed by transmission electron microscopy with measurement of axon diameter. Western blot was used to detect the protein expressions of p38 mitogen-activated protein kinases (p38MAPK), phosphorylated p38MAPK (p-p38MAPK), heme oxygenase 1 (HO-1), and nuclear factor erythroid 2-related factor 2 (Nrf2)., Results: MTT assay showed that the addition of SMC significantly promoted the proliferation of RSC96 cells, and the low concentration could achieve an effective effect, so the treatment method of group C was selected for the subsequent experiments; ROS immunofluorescence test showed that group B showed a significant increase in the intensity of ROS fluorescence compared with that of group A, and group C showed a significant decrease in the intensity of ROS fluorescence compared with that of group B ( P <0.05). Neuroelectrophysiological tests showed that the highest potential of CMAP in SMC group was significantly higher than that in PNI and Sham groups ( P <0.05). ELISA assay showed that the levels of IL-6, IL-17, and MDA in PNI group were significantly higher than those in Sham group, and the levels of IL-10, SOD, and CAT were significantly lower; the levels of IL-6, IL-17, and MDA in SMC group were significantly lower than those in PNI group, and the levels of IL-10, SOD, and CAT were significantly higher ( P <0.05). LFB staining and transmission electron microscopy showed that the myelin density and the diameter of axons in the SMC group were significantly higher than those of the PNI group and the Sham group ( P <0.05). Immunofluorescence staining showed that the fluorescence intensity of GFAP and MBP in the SMC group were significantly stronger than those in the PNI group and Sham group ( P <0.05). Western blot showed that the relative expressions of Nrf2 and HO-1 proteins in the SMC group were significantly higher than those in the PNI group and Sham group, and the ratio of p-p38MAPK/p38MAPK proteins was significantly higher in the PNI group than that in the SMC group and Sham group ( P <0.05)., Conclusion: SMC may inhibit oxidative stress and inflammation after nerve injury by up-regulating the Nrf2/HO-1 pathway, and then inhibit the phosphorylation of p38MAPK pathway to promote the proliferation of Schwann cells, which ultimately promotes the formation of myelin sheaths and accelerates the regeneration of peripheral nerves.

This study reviews the latest progress on the research of electrical stimulation（ES） in peripheral nerve regeneration, summarizes the parameters in preclinical experiments and discusses the effect on nerve regeneration. A detailed description is given in the study of conditioning electrical stimulation and nerve conduit scaffolding technology combined with ES, which have been hotly researched in recent years., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Editorial Department of Journal of Clinical Otorhinolaryngology Head and Neck Surgery.)

BACKGROUND: Traumatic neuroma is a common complication of peripheral nerve injury, and basic research on peripheral nerve repair and regeneration through a traumatic neuroma model is rarely reported. OBJECTIVE: To establish and identify a traumatic neuroma model. METHODS: The study was approved by the Laboratory Animal Ethical Committee of Chinese PLA General Hospital. Fifteen healthy Sprague-Dawley rats aged 8 weeks old were selected to expose the sciatic nerve under microscope, and the sciatic nerve was cut 1 em away from the posterior gluteal muscle branch using microscissors. The proximal nerve was sutured to the surrounding muscle with 11-0 microlines, and the distal nerve was left open and reflexed. After 3 weeks, ultrasonic and histological examinations were used to verify the formation of neuroma. RESULTS AND CONCLUSION: (1) Ultrasound: After 3 weeks of modeling, the proximal nerve showed obvious spindle enlargement, which was a hypoechoic parenchymal nodule without echo. (2) Gross observation: The proximal nerves were enlarged and slightly stiffened, with fibrous connective tissue hyperplasia and adhesion to the surrounding tissues. (3) Hematoxylin-eosin staining indicated hyperplasia of fibrous tissue and disorderly growth of nerve fibers in the tumor. Immunofluorescence staining (S100, NF200) revealed irregular hyperplasia of Schwann cells and nerve axons in the tumor. (4) These results suggest that the model of traumatic neuroma is successfully constructed. [ABSTRACT FROM AUTHOR]

Objective To explore the effects of fluoxetine on behavior and hippocampal dentate gyrus regeneration in rats with cerebral ischemia. Methods Thirty rats were selected to prepare the cerebral ischemia models, and 2 of them died due to anesthesia, 4 rats without hemiplegia were excluded, and the remaining 24 rats were randomly divided into the fluoxetine group and model group, with 12 in each; another 24 rats were randomly divided into the positive group and negative group, with 12 in each. Cerebral ischemia model was not prepared in the two groups, but normal saline was injected in the same anatomy; after 7 days of molding, the rats in the fluoxetine group and the positive group received 16 mg/(kg · d) fluoxetine orally for 3 weeks. The behavior of rats in each group was evaluated by balance beam experiment, the regeneration of hippocampal dentate gyrus in rats was observed by immunofluorescence technique. Results The drop rates of forepaw were 23.2% ± 2.4%, 25.7% ± 3. 2%, 13.6% ± 2. 1%, and 11. 1% ± 1. 9% in the fluoxetine group, model group, positive group and negative group, and the error rates of hind paw were 19. 5% ± 3. 1%, 22. 4% ± 3.4%, 8. 3% ± 1. 7% and 9. 7% ± 1. 8%, respectively, with statistically significant difference between the model group and the positive group and the negative group, and between the fluoxetine group and the model group (all P <0. 05). The number of DCX positive cells in hippocampal dentate gyrus of rats in the fluoxetine group, model group, positive group and negative group was 83.5 ± 4. 2, 61.5 ± 4. 7, 46.3 ± 3. 7, and 23.2 ± 3. 2, and the total length of dendrites was (898. 1 ±54. 2), (779. 3 ± 32. 1), (575. 2 ± 22. 3), and (218. 7 ± 17. 9) urn, respectively, with statistically significant difference between the model group and the positive group and the negative group, and between the fluoxetine group and the model group (all P < 0. 05). Conclusion F1uoxetine has no effect on the behavior of rats with cerebral ischemia, but it can promote nerve re generation in rats. [ABSTRACT FROM AUTHOR]

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BACKGROUND: Human amniotic membrane with low immunogenicity can reduce scar formation, inhibit inflammation and prevent angiogenesis. OBJECTIVE: To observe the effect of human amniotic membrane on repair and regeneration process after acute nerve injury. METHODS: Ninety adult male Sprague-Dawley rats provided by Laboratory Animal Center of Hebei Medical University were used for establishing the models of acute sciatic nerve injury and then randomly divided into amniotic membrane (nerve entrapment with amniotic membrane), chitosan (nerve entrapment with chitosan gel) and blank control (without any treatment) groups (n=30 per group). Gross, light microscope and transmission electric microscope observations, axon image analysis and electrophysiological examination were performed. RESULTS AND CONCLUSION: Gross, light microscope and transmission electric microscope observations revealed: compared with the blank control group, the mild limb swelling, neurohyperemia, and edema were observed in the amniotic membrane group. In addition, the adhesion with the surrounding tissue was mild in the amniotic membrane group, the inflammatory reaction was mild and there were few fibroblasts and newborn capillaries. In the amniotic membrane group, function of organelles was active, there were few fibroblasts and less collagen, and the repair time was short, which were similar with the chitosan group. The axon image analysis showed that thickness of the myelin sheath and the diameter of myelinated fibers in the amniotic membrane and chitosan groups were superior to those in the blank control group (P < 0.05). Neurophysiological stimulation showed that there was no significant difference in the nerve conduction velocity among groups. The amplitude was significantly different among groups (P < 0.05). The latent period in the amniotic membrane and chitosan groups was significantly shorter than that in the blank control group (P < 0.05). To conclude, amniotic membrane can provide a relatively stable microenvironment for nerve repair, reduce adhesion, inhibit inflammatory reaction, promote the repair and regeneration of nerve, and show good therapeutic effect. Amniotic membrane has a long retention time in vivo, which is beneficial to nerve regeneration and microenvironment maintenance, and contributes to the recovery of nerve function. Therefore, amniotic membrane is better than the chitosan. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of M2 microglia (M2-MG) transplantation on spinal cord injury (SCI) repair in mice., Methods: Primary MG were obtained from the cerebral cortex of 15 C57BL/6 mice born 2-3 days old by pancreatic enzyme digestion and identified by immunofluorescence staining of Iba1. Then the primary MG were co-cultured with interleukin 4 for 48 hours (experimental group) to induce into M2 phenotype and identified by immunofluorescence staining of Arginase 1 (Arg-1) and Iba1. The normal MG were harvested as control (control group). The dorsal root ganglion (DRG) of 5 C57BL/6 mice born 1 week old were co-cultured with M2-MG for 5 days to observe the axon length, the DRG alone was used as control. Forty-two 6-week-old female C57BL/6 mice were randomly divided into sham group ( n =6), SCI group ( n =18), and SCI+M2-MG group ( n =18). In sham group, only the laminae of T 10 level were removed; SCI group and SCI+M2-MG group underwent SCI modeling, and SCI+M2-MG group was simultaneously injected with M2-MG. The survival of mice in each group was observed after operation. At immediate (0), 3, 7, 14, 21, and 28 days after operation, the motor function of mice was evaluated by Basso Mouse Scale (BMS) score, and the gait was evaluated by footprint experiment at 28 days. The spinal cord tissue was taken after operation for immunofluorescence staining, in which glial fibrillary acidic protein (GFAP) staining at 7, 14, and 28 days was used to observe the injured area of the spinal cord, neuronal nuclei antigen staining at 28 days was used to observe the survival of neurons, and GFAP/C3 double staining at 7 and 14 days was used to observe the changes in the number of A1 astrocytes., Results: The purity of MG in vitro reached 90%, and the most of the cells were polarized into M2 phenotype identified by Arg-1 immunofluorescence staining. M2-MG promoted the axon growth when co-cultured with DRGs in vitro ( P <0.05). All groups of mice survived until the experiment was completed. The hind limb motor function of SCI group and SCI+M2-MG group gradually recovered over time. Among them, the SCI+M2-MG group had significantly higher BMS scores than the SCI group at 21 and 28 days ( P <0.05), and the dragging gait significantly improved at 28 days, but it did not reach the level of the sham group. Immunofluorescence staining showed that compared with the SCI group, the SCI+M2-MG group had a smaller injury area at 7, 14, and 28 days, an increase in neuronal survival at 28 days, and a decrease in the number of A1 astrocytes at 7 and 14 days, with significant differences ( P <0.05)., Conclusion: M2-MG transplantation improves the motor function of the hind limbs of SCI mice by promoting neuron survival and axon regeneration. This neuroprotective effect is related to the inhibition of A1 astrocytes polarization.

Diabetic peripheral neuropathy (DPN) is one of the common chronic complications of diabetes, resulting in neuropathy of spinal nerve, cranial nerve, and vegetative nerve. Diabetic distal symmetric multiple neuropathy is the most representative lesion of DPN, including symptoms of bilateral limbs pain, numbness, and paresthesia, etc. DPN is one of the main reasons causing diabetic foot ulcer (DFU). Schwann cells (SCs) are the primary glia cells of the peripheral nervous system, which play very important role in repairing after nerve injury. As the target cells of chronic hyperglycemia, SCs' functions, including the formation of myelin sheath, the secretion of neurotrophic factors, energy supplying for the axon, and the guidance of axon regeneration, etc., are damaged under the action of high glucose. The destroyed functions of SCs can inhibit the repair of damaged nerves and accelerate the progress of DPN. Therefore, if the damage of high glucose to SCs can be effectively reduced, it will provide a new way for the treatment of DPN and DFU and reduce the morbidity of DFU. This review focuses on the function of SCs and its relationship with DPN.

Acostic neuromas are considered to be one of the most difficult intracranial tumors to remove without producing additional neurological deficit. Despite the advances in intraoperative cranial nerve monitoring and neurosurgical techniques, postoperative nerve dysfunction is still an important issue with paralysis of the facial nerve. It’s known that the facial nerve is included in the peripheral nervous system. The process includes the treatments of facial palsy and the mechanisms of nerve regeneration， such as interactions between neural axons and Schwann Cells， changes of the growth cone， etc． It’s reviewed that advanced research on regenerating mechanism of injured facial nerve in this article. [ABSTRACT FROM AUTHOR]

Objective: The exosomes are membranous vesicles?which are derived from polycystic vesicles secreted by living cells.Their main functions include carrying and transporting substances. Schwann cells are one of the excellent seed cells in peripheral nerve regeneration. However, Schwann cells have a relatively poor migration ability which limite the biological effect on nerve regeneration.To investigate whether exosomes can promote Schwann cell migration under cell co-culture. Methods: In this experiment, we isolated and purified human umbilical cord stem cells’ exosomes and Schwann cells from rat sciatic nerve and then identified them.Subsequently, they were co-cultured in Transwell chamber to observe the migration rate of Schwann cells. Results: High expression of stem cell markers CD44(92.2 ± 3.6 %), CD73(99.1 ± 0.6 %) and low expression of mononuclear cell surface antigen CD14(0.5 ± 0.06%), hematopoietic stem cell surface antigen CD34(0.4 ± 0.07 %) in h UC-MSCs which were obtained by ultrahigh speed centrifugation.The exosomes were identified with high expression of CD81 and CD9. The identification of Schwann cells were factual and the purity of cells were 92.3 ± 2.7 %. All the cultured cells and exosomes were met the experimental requirements. And the exosomes can significantly promote Schwann cells’ migration under cell co-culture in Transwell chambers with dose relationship. Conclusions: The exosomes can accelerate Schwann cell migration obviously, which made Schwann cells more suitable for seed cells in nerve regeneration tissue engineering. [ABSTRACT FROM AUTHOR]

BACKGROUND: Y-27632 is a Rho-associated coil-formed protein kinase inhibitor that can regulate the self-renewal of stem cells, promote clonal formation and cell survival, and regulate and protect neuronal cell growth and development. How to improve the differentiation efficiency of embryonic stem cells into neuron-like cells is highly important for nerve injury repair and nerve regeneration. OBJECTIVE: To investigate the effect of Y-27632 on the differentiation efficiency and function of human embryonic stem cells into neuron-like cells. METHODS: After resuscitation, human embryonic stem cells at passage 16 were subjected to morphological observation and staining identification. The embryoid bodies were prepared by suspension culture, and after 8 days of incubation, the cells were cultured in Sato medium containing different concentrations of Y-27632 (0, 5, 10, 20, 40 μmol/L) for 10 days and identification by staining. After induction for 18 days, the differentiation efficiency and neurite outgrowth were identified by immunofluorescence staining. RESULTS AND CONCLUSION: The human embryonic stem cells co-expressed Oct4 and SSEA-3 stem cell specific markers. After suspension culture for 8 days and further adherent culture for 10 days, the cells could be differentiated into neuron-like cells with neurogenic morphology and expressing Tuj-1. Y-27632, especially at a concentration of 10 μmol/L, not only promoted cell proliferation (a significant increase in adherent cells an Tuj-1 positive cells), but also facilitated cell differentiation into neurons. Immunofluorescence staining findings showed that 10 μmol/L Y-27632 significantly increased the number of Tuj-1 positive cells and neurites and the length of neurites after 18 days of differentiation. These results indicate that Y-27632 not only promotes the differentiation of human embryonic stem cells into neuron-like cells, but also accelerates neurite outgrowth. [ABSTRACT FROM AUTHOR]

BACKGROUND: Interleukin-17A has been shown to play an important role in nerve regeneration following corneal injury. OBJECTIVE: To investigate the effect of interleukin-17A on mouse nerve regeneration after optic nerve injury. METHODS: The interleukin-17A-overexpressed adenovirus vector (AV-IL-17A-GFP) was constructed and purified. Adenoviruses with green fluorescent protein (AV-GFP) served as control group. PC12 cell lines were transfected with adenoviruses and the expression efficiency of IL-17A were detected by ELISA. The adenovirus was intravitreally injected into the mouse vitreous body, and the expression level of IL-17A in the optic nerve was determined by immunofluorescence. Afterwards, a mouse model of optic nerve injury was established to observe the nerve regeneration. RESULTS AND CONCLUSION: ELISA results showed that IL-17A was highly expressed in the PC12 cell lines transfected with AV-IL-17A-GFP compared with the control group. Immunofluorescence results revealed that IL-17A was expressed in vivo successfully. There was a significant increase in the number of regenerated axons in the AV-IL-17A-GFP group compared with the control group (P < 0.05). To conclude, AV-IL-17A-GFP can be expressed in the mature neurons in vivo and promote the axon regeneration after optic nerve crush injury in mice. [ABSTRACT FROM AUTHOR]

BACKGROUND: In recent years, neural stem cells, adipose tissue derived mesenchymal stem cells, muscle derived stem cells and induced pluripotent stem cells have been applied in the treatment of peripheral nerve injuries. However, the treatment of peripheral nerve injury by autologous peripheral blood mononuclear cells has rarely been reported. OBJECTIVE: To investigate the efficacy of autologous peripheral blood mononuclear cells in the treatment of high radial nerve injury. METHODS: From April 2011 to September 2015, 12 cases of radial nerve injury in the middle arm were treated. Preoperatively peripheral blood mononuclear cells were mobilized, and then 15 mL of mononuclear cell suspension was prepared on the operation day. Radial nerves scheduled for anastomosis were surgically explored and subjected to end-end anastomosis using outer membrane suturing under microscope. The anastomotic site of the nerve was enveloped with gelatin sponge soaked with 5 mL of autologous peripheral blood mononuclear cell suspension. The remaining 10mL of cell suspension was used for a multi-point injection into the local muscles, 0.5 mL at each point. Thereafter, the deep fascia and the incision were sutured in sequence. Postoperative antibiotics were used to prevent infection for 48 hours, and upper limb immobilization lasted for 4 weeks. Performance of rehabilitation exercise was guided. During the follow-up, wrist dorsal extension and muscle strength of extensor carpi ulnaris and extensor digitorum communis were detected to evaluate the therapeutic efficacy. RESULTS AND CONCLUSION: All the patients were followed up for 15 to 36 months, with an average of 17 months. Efficacy was excellent in 9 cases, good in 2 cases, fair in 1 case and poor in 0 case. The excellent and good rate was 92%. The wrist dorsal extension could achieve the functional needs, and the thumb dorsal extension and finger extension basically met the functional requirements. It is suggested that autologous peripheral blood mononuclear cell transplantation can achieve good outcomes in the treatment of high radial nerve injury. [ABSTRACT FROM AUTHOR]

BACKGROUND: Gastrodin has been shown to inhibit the in vivo astrocyte activation after injury, improve the microenvironment of spinal cord injury (SCI), and reduce secondary injuries. OBJECTIVE: To observe the effects of gastrodine on the neural functional recovery and glial fibrillary acidic protein in a rat model of clamping-induced SCI. METHODS: Forty-eight adult Sprague-Dawley rats were randomly divided into three groups, and the models of clamping-induced SCI were established. The rats in sham group were only subjected to laminectomy; gastrodine group was given 100 mg/kg•d gastrodine; the sham and SCI groups were given equal volume of normal saline. The function recovery of spinal cord was evaluated by Basso, Beattie, Bresnahan (BBB) scores, and Rivlin inclined plane experiment at postoperative 1, 3, 7, 14, 21 and 28 days. The morphological changes of spinal cord were observed after perfusion at 28 days, expression level of glial fibrillary acidic protein was detected by immunofluorescence, and changes of Nissl body were observed through Nissl staining. RESULTS AND CONCLUSION: BBB and Rivlin inclined plane scores in each group were significantly decreased postoperatively, and the scores then increased with time; the scores at each time point in the sham group were significantly higher than those in the other groups (P < 0.05); the scores in the gastrodine group were significantly higher than those in the SCI group from day 3 (P < 0.05). At postoperative 28 days, the expression level of glial fibrillary acidic protein was the lowest in the sham group, followed by gastrodine group, and the highest in the SCI group (P < 0.05). In the gastrodine and SCI groups, Nissl bodies were slightly stained partially dissolved, and the account of Nissl bodies in this two groups was less than that in the sham group (P < 0.05), but the gastrodine group had significantly more Nissl bodies than the SCI group (P < 0.05). The spinal cord in the sham group revealed the complete structure; in the SCI group, the structure of spinal cord was in disorder, syringomyelia formatted, and the gray-white matter boundary was obscure; gastrodine group showed smaller syringomyelia and gray-white matter boundary were clear. These results show that gastrodin can inhibit the proliferation of astrocytes after SCI, play neuroprotection, and improve motor function. [ABSTRACT FROM AUTHOR]

BACKGROUND: Previous studies have shown that traumatic brain injury can promote the regeneration of peripheral nerve by reducing scar collagen in nerve endings. OBJECTIVE: To investigate the effect of brain injury at different locations on the ipsilateral rat sciatic nerve regeneration. METHODS: Ninety-nine healthy male Sprague-Dawley rats were equivalently randomized into three groups: group A, right sciatic nerve transection; group B, right sciatic nerve transection combined with right brain injury; and group C, right sciatic nerve transection combined with left brain injury. All of transected nerves were sutured under microscope. Classical Feeney method was used to establish a model of traumatic brain injury. At 4, 6, 8, 10 and 12 weeks after modeling, the sciatic functional index (SFI) was calculated by measuring footprint. At 4, 8 and 12 weeks after modeling, the bilateral gastrocnemius were harvested for determining wet weight and calculate wet weight ratio, followed by acetylcholinesterase staining at the motor end plate to detect the absorbance values. At 4, 8 and 12 weeks after modeling, fluoro-gold retrograde tracing was used to trace L4-5 vertebrae for 1 week, and the number of spinal cord anterior horn motor neurons positive for fluoro-gold was detected and calculated by fluorescence microscope. RESULTS AND CONCLUSION: The SFI value in each group was gradually improved with time. The SFI value was significantly higher in the groups B and C than the group A at 4 and 6 weeks after modeling (P < 0.05), and was further improved in the group B at 8 weeks compared with the groups A and C (P < 0.05). The wet weight ratio of gastrocnemius showed no significant difference among groups at 4 weeks after modeling (P > 0.05), and the group B showed a significantly higher wet weight ratio than the other groups from the 8th week (P < 0.05). Compared with the groups A and C, the absorbance values of motor endplate in group B appeared to be a significant increase at the beginning of the 8th week (P < 0.05). At 4 and 6 weeks after modeling, the number of spinal cord anterior horn motor neurons positive for fluoro-gold was significantly nigher in the groups B and C than in the group A, and the number was significantly higher in the group B than the groups A and C at 12 weeks (all P < 0.05). These finding manifest that brain injury can promote the repair of ipsilateral sciatic nerve injury, thus proving theoretical reference for unveiling the mechanism by which traumatic brain injury promotes peripheral nerve regeneration. [ABSTRACT FROM AUTHOR]

Objective To investigate the influence of velvet antler polypeptides (VAP)-PLGA compound membrane formed from VAP and copolymer (PLGA) of polylactic acid (PLA) and polyglycolic acid (PGA) on regeneration of sciatic nerve in rats. Methods Healthy male Wistar rats (n=36) were randomly divided into 4 groups (each n=9). The sciatic nerve of rat was revealed by operation, and was not treated in sham-operation group after isolating the nerve and sewed up directly broken ends in model group after cutting the nerve. The sciatic nerve of rat was sewed up and wrapped up with PLGA compound membrane in control group and the nerve was sewed up and wrapped up with VAP-PLGA compound membrane in treatment group. The samples were collected respectively on the 2nd, 4thand 6th weeks after the operation and given histological and immunohistochemical observation and detection. Results The histological observation showed that nervous axon was normal in sham-operation group at 3 time points. The quantity of medullated fibers was significantly more, and axon regeneration rate and maturity of regenerated axon were significantly higher in treatment group than those in model group and control group (P<0.05) at 3 time points. The immunohistochemical detection showed that the antigen staining and antigen expressions of transforming growth factor β (TGF-β) and insulin-like growth factor (IGF) in regenerated nerve fiber axon and myelin sheath were significantly higher in treatment group than those in sham-operation group, model group and control group (P<0.05). Conclusion VAP-PLGA compound membrane can provide a microenvironment and neuroactive factors required by neural restoration, and promote the regeneration of peripheral nerve, which is an ideal biological material for neural restoration. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To evaluate the effect of fresh amniotic membrane on the regeneration of tinjured peripheral nerve. METHODS: Sixty healthy Sprague-Dawley rats were randomly divided into three groups (n=20 per group) after constructing a model of sciatic nerve injury of the unilateral leg. In group A, the nerve was wrapped with fresh human amnion at the anastomosis end after the repair of nerve. In group B, the nerve was wrapped with biofilm at the anastomosis end after the repair of nerve. In group C, no treatment was conducted after the repair of nerve (blank control). The effects were evaluated by anatomical observation, light microscope observation, immunohistochemical detection (2, 4, 8, 12 weeks after surgery), transmission electron microscope observation, axon imaging analysis, action potential detection, and sciatic nerve function index (4, 8, 12 weeks after surgery). RESULTS AND CONCLUSION: (1) Gross observation. The amniotic membrane and biofilm were absorbed partially at postoperative 2 weeks, mostly at postoperative 4 weeks and completely at postoperative 8 weeks. In the groups A and B, the nerve was adhered slightly and loosely to the surrounding tissues, with a fair range of motion. In the group C, the nerve was tightly adhered to the surrounding tissues, with a poor range of motion. (2) Observation under light microscope. The nerve regeneration was better in the groups A and B than group C at 2, 4, 8, 12 weeks postoperatively. (3) Observation under electron microscope. Regenerated nerve fibers were rarely seen and lamellar structures were unclear in the three groups at 4 weeks postoperatively. Then, increased regenerated nerve fibers, thickened myelin sheath, clear lamellar structure and enlarged axon diameter were found in the groups A and B compared with the group C at 8 and 12 weeks postoperatively. (4) Immunohistochemical detection. The expression and distribution of S-100 protein in the groups A and B were better than those in the group C. (5) Axon image analysis. Groups A and B were superior to the group C in the diameter of myelinated nerve fibers, thickness of myelin sheath and number of regenerated nerve fibers. There was a significant difference by statistical analysis (P < 0.05). (6) Electrophysiological examination. Shorter latency period, higher amplitude and faster nerve conduction velocities were observed in the groups A and B compared with the group C (P < 0.05). (7) The sciatic function index. The sciatic function index in group A or B was significantly higher than that in group C (P < 0.05). To conclude, the human amniotic membrane can reduce adhesion between the damaged nerve and surrounding tissues, and prevent scarring at the anastomosis end. In addition, it promotes the regeneration of nerve fibers, increase axon diameter and myelin sheath thickness, and ease inflammatory and immune responses at the neural incision. [ABSTRACT FROM AUTHOR]

Artificial nerve guidance conduits (NGCs) are synthetic nerve grafts that are capable of providing the structural and nutritional support for nerve regeneration. The ideal NGCs have plenty of requirements on biocompatibility, mechanical strength, topological structure, and conductivity. Therefore, it is necessary to continuously improve the design of NGCs and establish a better therapeutic strategy for peripheral nerve injury in order to meet clinical needs. Although current NGCs have made certain process in the treatment of peripheral nerve injury, their nerve regeneration and functional outcomes on repairing long-distance nerve injury remain unsatisfactory. Herein, we review the nerve conduit design from four aspects, namely raw material selection, structural design, therapeutic factor loading and self-powered component integration. Moreover, we summarize the research progress of NGCs in the treatment of peripheral nerve injury, in order to facilitate the iterative updating and clinical transformation of NGCs.