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Objective: To investigate therapeutic effect and mechanism of sanguinarine on postherpetic neuralgia (PHN) rats by modulating C-X-C chemokine ligand 12 (CXCL12) /C-X-C chemokine receptor 4 (CXCR4) signaling pathway. Methods: SD rats were randomly grouped into control group, model group, low-dose (50 mg/kg) sanguinarine group, high-dose (100 mg/kg) sanguinarine group, NUCC-390 (CXCL12/CXCR4 signal activator, 2.2 mg/kg) group, high-dose (100 mg/kg) sanguinarine+NUCC-390 (2.2 mg/kg) group, with 10 rats in each group. Rats in model group and drug-treated groups were injected with resin toxin (RTX) by intraperitoneal injection to induce PHN model, rats in control group were intraperitoneally injected with an equal dose of normal saline containing 10% Tween 80 and 10% ethanol. After treatment of sanguinarine and NUCC-390, symptoms of long-term spontaneous pain, mechanical hyperalgesia and thermal hyperalgesia were detected, number of spontaneous paw withdrawal reflexes, paw withdrawal threshold to mechanical stimulation (PWMT), and response latency to thermal stimulation (PWTL) were compared; spinal cord nerve cell apoptosis was detected by TUNEL staining; ELISA was used to detect levels of inflammatory factors TNF-α, IL-1β, cyclooxygenase-2 (COX-2) in rat spinal cord tissue and serum; Western blot was used to detect expressions of CXCL12/CXCR4 pathway-related proteins in spinal cord tissues of rats in each group. Results: Compared with control group, PWMT of model group was obviously decreased (P<0.05), number of spontaneous foot withdrawal reflexes, PWTL, spinal nerve cell apoptosis index, levels of TNF-α, IL-1β, COX-2 in spinal cord tissue and serum, and protein expressions of CXCL12 and CXCR4 in spinal cord tissue were obviously increased (P<0.05) . Compared with model group, PWMT of rats in low-dose sanguinarine group and high-dose sanguinarine group was increased (P<0.05), number of spontaneous foot withdrawal reflexes, PWTL, spinal nerve cell apoptosis index, levels of TNF-α, IL-1β, COX-2 in spinal cord tissue and serum, and protein expressions of CXCL12 and CXCR4 in spinal cord tissue were all decreased (P<0.05) ; PWMT of rats in NUCC-390 group was decreased (P<0.05), number of spontaneous foot withdrawal reflex, PWTL, spinal nerve cell apoptosis index, levels of TNF-α, IL-1β, COX-2 in spinal cord tissue and serum, and protein expressions of CXCL12 and CXCR4 in spinal cord tissue were increased (P<0.05). Compared with high-dose sanguinarine group, PWMT of rats in high-dose sanguinarine+NUCC-390 group was decreased (P<0.05), number of spontaneous foot withdrawal reflex, PWTL, spinal nerve cell apoptosis index, levels of TNF-α, IL-1β, COX-2 in spinal cord tissue and serum, and protein expressions of CXCL12 and CXCR4 in spinal cord tissue were increased (P<0.05). Conclusion: Sanguinarine can reduce expression of inflammatory factors by down-regulating CXCL12/CXCR4 signaling pathway, thereby preventing occurrence of inflammatory response in PHN rats, inhibiting apoptosis of spinal nerve cells, and finally reducing long-term spontaneous pain, mechanical allodynia and thermal hypoalgesia in rats. [ABSTRACT FROM AUTHOR]

Copyright of Machine Tool & Hydraulics is the property of Guangzhou Mechanical Engineering Research Institute (GMERI) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the mechanism of liraglutide (Lira) intervention on oxidative stress, mitochondrial function and autophagy damage in human neuroblastoma (SH-SY5Y) cells. Methods: SH-SY5Y cells were divided into control group, high glucose (HG) group, HG+LI-L group, HG+LI-H group HG+LI-H+3-methyladenine (3MA) group. The cell proliferation ability, the levels of Glu, malondialdehyde (MDA), adenosine triphosphate (ATP), superoxide dismutase (SOD), Cell apoptosis, reactive oxygen species (ROS) level, mitochondrial membrane potential. The expression and localization of microtubule-associated protein 1 light chain 3 (LC3B), p62, The expression of phosphatidylinositol 3-kinase (PI3K), p-PI3K, mammalian rapamycin target protein (mTOR) p-mTOR, protein kinase B (Akt) and p-Akt protein were detected. Results: Compared with HG group, the cell proliferation activity in HG+LI (500 nM) group was the most significant, Glu and MDA decreased and SOD increased in HG+LI (500 nM) group, the cell viability, ATP and SOD were increased, and the apoptosis rate, ROS fluorescence intensity, Glu, MDA and JC-1 were decreased in HG+LI-L group and HG+LI-H group, and the cell viability, ATP and SOD in HG+LI-H group were higher than those in HG+LI-L group, and the apoptosis rate, ROS fluorescence intensity, Glu, MDA and JC-1 were lower than those in HG+LI-L group, p-mTOR and p62 proteins expression were decreased, p-PI3K, p-Akt and LC3B proteins expression were increased in the HG+LI-H group (P<0.05). Compared with control group, Glu, MDA, apoptosis rate, ROS fluorescence intensity, Glu, MDA, JC-1, P-mTOR and p62 protein expression in HG group increased, while SOD, ATP, cell survival rate, p-PI3K, p-Akt and LC3B protein expression decreased (P<0.05). Compared with HG+LI-H group, the cell viability, ATP, SOD, p-PI3K, p-Akt and LC3B protein expression were decreased, and the apoptosis rate, ROS fluorescence intensity, Glu, MDA JC-1, p-mTOR and p62 protein expression were increased in HG+LI-H+3MA group (P<0.05). Conclusion: Lira may reduce oxidative stress in SH-SY5Y cells in a dose-dependent manner, improve mitochondrial function and PI3K/AKT/mTOR autophagy pathway, Play a role in resist apoptosis and protect nerve cells. [ABSTRACT FROM AUTHOR]

AIM: To investigate the role and mechanism of histone demethylase lysine-specific demethylase 5A (KDM5A) in regulating the Notch signaling pathway in particulate matter 2. 5 (PM2. 5)-induced cortical damage in offspring mice. METHODS: A pregnancy PM2. 5 exposure model was established using intratracheal nebulization. Pregnant mice were randomly divided into PBS control group and PM2. 5 exposure group. The cortices of offspring mice were isolated 14 d after birth. Golgi staining, electron microscopy and other methods were used to detect damage to neurons and chromatin in the cortex. Western blot, RT-qPCR and immunofluorescence staining were used to detect the mRNA and protein expression of KDM5A in the cortex, and the distribution of KDM5A co-localized with neural cells. A PM2. 5-treated PC12 cell injury model was established to detect changes in cell viability and the expression of proteins related to cell proliferation and apoptosis. Further, Western blot, RT-qPCR and immunofluorescence staining were used to detect the mRNA and protein expression of KDM5A, the distribution of KDM5A co-localized with neurons, and changes in the protein level of histone H3K4me3. Bioinformatics methods were used to predict the interaction between KDM5A and Notch1, which was further validated by transfection experiments. In both in vivo and in vitro PM2. 5 exposure models, changes in key molecules of the Notch signaling pathway and the co-expression of Notch1 with neural cells in the cortices of 14-day-old offspring mice and PC12 cells were detected. RESULTS: Prenatal PM2. 5 exposure during pregnant led to a reduction in the number of neurons and decreased dentritic complexity in the cerebral cortex of offspring at 14 d after birth. It also caused abnormal chromatin condensation within neuronal nuclei, decreased mRNA and protein expression of KDM5A protein in the cortex, increased H3K4me3 protein levels (P<0. 05), and a significant reduction in KDM5A/NeuN double-positive cells. Exposure to PM2. 5 also resulted in decreased viability and proliferation, and increased apoptosis of PC12 cells, with reduced expression of KDM5A mRNA and protein, increased H3K4me3 protein expression (P<0. 05), and a reduction in the number of KDM5A/MAP-2 double-positive cells. Bioinformatics analysis and transfection experiments in PC12 cells revealed that Notch1 is a downstream target gene of KDM5A. Further in vivo and in vitro experiments found that PM2. 5 exposure lead to decreased mRNA and protein expression of key Notch signaling molecules Notch1, Jagged1 and Hes1, and reduced numbers of Notch1/NeuN and Notch1/MAP-2 double-positive cells. CONCLUSION: Exposure to PM2. 5 can lead to abnormal expression of KDM5A in the offspring's cerebral cortex, which may cause neuronal damage by down-regulating the Notch signaling pathway, a downstream target. This could be one of the significant factors contributing to the neurodevelopmental disorders in offspring exposed to PM2. 5 during pregnancy. [ABSTRACT FROM AUTHOR]

[Objective] This study aims to investigate the anti-depression effects of enzymatic hydrolysates of mulberry leaf flavonoids (EMLF). [Methods] EMLF was prepared and its components were analyzed by UPLC-MS. A zebrafish model of depression was induced by 40 mg/L reserpine. Six groups were designed, including the control, model, fluoxetine, L-EMLF (20 µg/mL), M-EMLF (40 µg/mL), and H-EMLF (80 µg/mL) groups. Behavioral tests, including the new tank test and the light-dark box test, were conducted. The structural changes in the brain tissue of zebrafish in each group were observed by HE staining. The mRNA levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), tryptophan hydroxylase-2 (TPH-2), and 5-hydroxytryptamine 2A (5-HT2A) receptor in the brain tissue were determined by q-PCR. The activity of superoxide dismutase (SOD) and the level of reactive oxygen species (ROS) in the brain tissue of zebrafish were measured. Metabolomics analysis was performed to identify differential metabolites and associated metabolic pathways. [Results] UPLC-MS identified 10 flavonoid aglycone compounds. Reserpine (40 mg/L) induced depression-like behaviors in zebrafish, while EMLF alleviated the bottom-dwelling and dark-preference behaviors, restored the orderly arrangement of nerve cells in the midbrain region, and increased the cell number. EMLF treatment down-regulated the mRNA levels of IL-1β, TNF-α, and 5-HT2A while up-regulating the mRNA level of TPH-2. In addition, EMLF increased the SOD activity and reduced the ROS level. Metabolomics analysis revealed that EMLF significantly regulated 24 differential metabolites, primarily affecting purine metabolism, arginine and proline metabolism, tryptophan metabolism, and riboflavin metabolism. [Conclusion] EMLF effectively alleviated reserpine-induced depression in zebrafish, potentially by regulating the tryptophan metabolism, purine metabolism, and arginine and proline metabolism. [ABSTRACT FROM AUTHOR]

Copyright of Biology Teaching is the property of East China Normal University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Electroencephalography (EEG), which can intuitively monitor and record the discharge activities of neuronal groups in the brain, is a crucial scientific and clinical diagnostic technique in the field of neuroscience. EEG has been developed and innovated for nearly a century, and it offers advantages of non-invasiveness, convenience, real-time, and continuity. The rapid advancement and multidisciplinary integration of computer technology and other imaging techniques has led to the application of EEG technology in a wide range of areas, including epilepsy, sleep disorders, and critical care. The purpose of this article is to enhance clinical comprehension and implementation of EEG technology by reviewing its development history, clinical applications, and future prospects. [ABSTRACT FROM AUTHOR]

BACKGROUND: We have successfully isolated and cultured neonatal mouse cerebrospinal fluid-contacting neurons in vitro, but there is no study that reports an effective method for isolating and culturing high-purity adult mouse cerebrospinal fluid-contacting neurons. There is no study on whether the self-renewal ability of cerebrospinal fluid-contacting neurons changes with age. OBJECTIVE: To establish a method for isolating and culturing high-purity adult mouse cerebrospinal fluid-contacting neurons in vitro, and to characterize the self-renewal ability of adult mouse cerebrospinal fluid-contacting neurons and neonatal mouse cerebrospinal fluid-contacting neurons in vitro. METHODS: Primary cells containing cerebrospinal fluid-contacting neurons were isolated from the cervical medulla of adult mouse (3 months of age) in adherent culture and transfected with lentivirus fused with multimodal imaging genes. High-purity adult mouse cerebrospinal fluid-contacting neurons were obtained by puromycin screening in suspension culture in complete medium. The expression of neural stem cell markers Nestin and SOX2 was detected by immunofluorescence in adult mouse cerebrospinal fluid-contacting neurons, and the ability of adult mouse cerebrospinal fluid-contacting neurons to form spheres and pass on in vitro was observed. An equal number (5×10³ /mL) of passage 3 adult mouse and neonatal mouse cerebrospinal fluid-contacting neurons were divided into two groups under the same conditions and inoculated into ultra-low adhesion plates containing complete medium in suspension culture at 5% CO2, 37°C thermostat, respectively. The self-renewal capacity of adult mouse and neonatal mouse cerebrospinal fluid-contacting neurons was characterized by in vitro spheroid formation, CCK8 assay, qPCR, and western blot assay. RESULTS AND CONCLUSION: (1) High-purity cerebrospinal fluid-contacting neurons were successfully isolated from adult mouse, which expressed Nestin and SOX2 in vitro, and were able to form neurospheres and pass on continuously. (2) The in vitro self-renewal ability of cerebrospinal fluid-contacting neurons in adult mouse was significantly weaker than that of neonatal mouse, and the neurospheres formed by day 4 of cell culture in neonatal mouse were about 150 μm in diameter, whereas the neurospheres formed by adult mouse tactile neurons were only 40 μm in diameter (P < 0.000 1). (3) CCK8 proliferation assay showed that the proliferative activity of adult mouse cerebrospinal fluid-contacting neurons was significantly weaker than that of neonatal mouse at all time points after culture (P < 0.000 1). (4) qPCR and western blot assay revealed that the mRNA (P < 0.000 1) and protein expression levels (P < 0.01) of Nestin and SOX2 in cerebrospinal fluid-contacting neurons of adult mouse were significantly decreased compared with those of neonatal mouse. (5) The above results indicated that the self-renewal ability of cerebrospinal fluid-contacting neurons in adult mouse was significantly weaker than that of neonatal mouse in vitro. [ABSTRACT FROM AUTHOR]

BACKGROUND: Stem cells can promote nerve regeneration, repair damaged nerves, inhibit inflammation and apoptosis of nerve cells, and provide a new way for the treatment of Alzheimer’s disease. OBJECTIVE: To make a bibliometrical analysis of the articles on stem cell therapy for Alzheimer’s disease published internationally from 2004 to 2023, in order to reveal the research hotspot and trend of stem cell therapy for Alzheimer’s disease. METHODS: From the Web of Science Core Collection database, by using Excel, VOSviewer, and Citespace software, the annual number of publications, countries, institutions, journals/co-cited journals, authors, and keywords of articles related to stem cells and Alzheimer’s disease published from January 1, 2004 to October 31, 2023 were visually analyzed. RESULTS AND CONCLUSION: A total of 3 521 core papers were included, and the number of published papers increased year by year. The United States is the country with the most papers. Harvard Medical School is the most prolific institution. Maiese kenneth is the author with the most papers. International Journal of Molecular Sciences has the most papers in this field. The journal PLoS One published the most citations. At present, the field of stem cell therapy for Alzheimer’s disease focuses on pathophysiological mechanism and animal experimental research, and “neurogenesis”, “oxidative stress”, “extracellular vesicles”, and “mesenchymal stem cells” are the research trends in this field. Stem cell therapy for Alzheimer’s disease has broad prospects. In the future, exchanges and cooperation between institutions and authors should be strengthened to further explore the main mechanism of stem cell therapy for Alzheimer’s disease, solve possible clinical problems such as immune rejection, effectiveness, and safety, and further tap the potential of stem cells in the treatment of Alzheimer’s disease. [ABSTRACT FROM AUTHOR]

BACKGROUND: Primary cortical neurons and microglial cells play a crucial role in exploring cell therapies for neurological disorders, and most of the current methods for obtaining the two types of cells are cumbersome and require separate extraction. It is therefore crucial to find a convenient and rapid method to extract both types of cells simultaneously. OBJECTIVE: To explore a novel method for simultaneous extraction of primary cortical neurons and microglial cells. METHODS: Newborn suckling SD rats were taken within 24 hours. The brain was removed and placed in a dish with DMEM, and the pia mater was removed for later use. Primary neurons were extracted from the same brain tissue, and then the remaining brain tissue was used to extract microglial cells. The whole process was performed on ice. Extraction and culture steps of primary cortical neurons: The cerebral cortex was taken 2.0-3.0 mm with forceps, and the tissue was digested with papain for 20 minutes. After aborting digestion, the blown tissue presented an adherent tissue suspension. The supernatant cell suspension was obtained, filtered, and dispensed into 15 mL centrifuge tubes. After centrifugation and re-suspension, the cells were inoculated onto 6-well plate crawls coated with L-polylysine. Neuronal morphology was observed at 1-day intervals, and staining could be performed for identification using immunofluorescence staining of MAP2 and β-Tubulin by day 7. Microglia extraction and culture steps: The remaining brain tissue at 8-10 mm thick was subjected to microglial cell extraction, digested by trypsin for 20 minutes. After digestion was stopped, the tissue was blown to a homogenate, and then the homogenate was transferred to the culture bottle for culture. On day 14, the culture flasks were sealed and subjected to constant temperature horizontal shaking for 2 hours. Microglial cells were shed in the supernatant. Purified microglial cells were taken and continued to be cultured for 3 days for identification by Iba1 immunofluorescence staining. RESULTS AND CONCLUSION: After 24 hours of culture, the neurons were adherent to the wall, the cytosol was enlarged, and some neurons developed synapses. After 3 and 5 days of culture, the cytosol was further enlarged, and most of the neurons were in the form of synapses, and some neurons were growing in clusters. On day 7, neuronal synapses were prolonged and thickened, and they were connected with each other to form a network. The neurons were identified by β-Tubulin and MAP2 immunofluorescence staining. The cells grew close to the wall on day 1 of culture. On days 3, 5, and 7, the density of microglial cells was small, and the cell morphology was bright oval or round, but the cells basically grew in clumps on the upper layer of other cells. On day 10, the density of microglial cells increased significantly. On day 14, microglial cells grew in dense clumps on the upper layer of other cells, and then they could be isolated and purified. The isolated and purified cells were taken and re-cultured to day 3 and identified as microglial cells by Iba1 immunofluorescence; their purity was greater than 95%. The results show that primary cortical neurons and microglial cells obtained by this method after extraction and culture are of high purity, good morphology, and high viability. [ABSTRACT FROM AUTHOR]

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Objective To observe the immediate analgesic effect and mechanism of Three-Manipulation and Three-Acupoint tuina on rats with sciatic nerve injury. Methods Twenty-seven Sprague-Dawley (SD) rats were randomly divided into the sham operation group, model group, and tuina group, with nine rats in each group. In the model and tuina groups, we established the models of mild chronic constriction injury of sciatic nerve to simulate clinical neuropathic pain, while in the sham operation group, rats only underwent nerve exposure and suturing. On the 7th day after modeling, rats in the tuina group received Three-Manipulation and Three-Acupoint tuina therapy, with each acupoint treated for 1 minute using three techniques (9 minutes in total). Rats in the sham operation and model groups were only restrained without intervention for 9 minutes. Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were measured before modeling (T1), after modeling but before tuina (T2), and after tuina (T3) to evaluate the immediate analgesic effect. After evaluation, lumbar enlargement segment spinal dorsal horn tissues were collected. Western blotting was used to detect the expression of brain-derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB), and potassium-chloride cotransporter 2 (KCC2) proteins, and immunofluorescence was used to detect the ionized calcium-binding adapter molecule 1 (IBA-1), cluster of differentiation 68 (CD68), and cellular oncogene Fos (c-Fos) expression. Results Compared with the sham operation group, the model group showed significantly lower MWT and TWL at both T2 and T3 (both P<0. 05). However, the tuina group had significantly higher MWT and TWL at T3 as compared with the model group (both P<0. 05). The expression levels of BDNF and TrkB in the dorsal horn were higher, and KCC2 expression was lower in the model group than in the sham operation group (all P<0. 05). Compared with the model group, the tuina group exhibited lower BDNF and TrkB expression but higher KCC2 expression (all P<0. 05). No significant differences were found in the expression of BDNF, TrkB, or KCC2 between the sham operation and tuina groups (all P>0. 05). Additionally, the fluorescence intensity of IBA-1, CD68, and c-Fos was higher in the model group than in the sham operation group (all P<0. 05), while CD68 and c-Fos expression was lower in the Tuina group as compared with the model group (both P>0. 05). Conclusions Three-Manipulation and Three-Acupoint tuina demonstrates a good immediate analgesic effect in rats with sciatic nerve injury. The underlying mechanism may involve modulating microglia-neuron interactions and altering the activation state of microglia. [ABSTRACT FROM AUTHOR]

Objective: To investigate neuroprotective effect of alpinetin on ischemic stroke (IS) rats by regulating Shh/Glil signaling pathway. Methods: Fifteen rats were randomly collected as control group, remaining rats were used to construct an IS model. Rats that successfully modeling were randomly grouped into model group, alpinetin group (5 mg/kg), Shh/Glil signaling pathway inhibitor cycloparamide group (15 mg/kg) and alpinetin+cycloparamide group (5 mg/kg alpinetin+15 mg/kg cycloparamide), with 15 rats in each group, and administered once a day for two consecutive weeks, control group and model group were given equal amounts of physiological saline. Zea-Longa scoring method was applied to evaluate neural function; ELISA was applied to detect inflammatory factors levels; mass of brain tissue was weighed and water content of brain tissue was calculated; TTC staining was applied to measure volume of cerebral infarction; HE staining was applied to observe nerve cell damage; TUN EL staining was applied to detect neuronal apoptosis; qRT-PCR and Western blot were used to detect mRNA and protein expressions of Shh and Glil. Results: There were no abnormalities in hippocampal tissue of control group, while hippocampal tissue structure of model group rats was abnormal, with disordered cell arrangement and nuclear pyknosis of nerve cells, cell damage rate, Zea-Longa score, infarct volume, IL-1β, IL-6, TNF-α, brain tissue water content, and cell apoptosis rate in model group were obviously higher than control group (P< 0.05), mRNA and protein levels of Shh and Glil were obviously decreased (P<0.05) ; compared with model group, cells in alpinetin group were arranged more neatly, and phenomenon of neuronal cell nucleus pyknosis was improved, cell damage rate, Zea-Longa score, infarct volume, IL-1β, IL-6, TNF-α, brain tissue water content, and cell apoptosis rate were obviously decreased (P<0.05), mRNA and protein levels of Shh and Glil were obviously increased (P<0.05), trend of above indicators in cyclophosphamide group was opposite, ciclopramide reversed neuroprotective effect of alpinetin on IS rats. Conclusion: Alpinetin may exert neuroprotective effects on IS rats by activating Shh/Glil signaling pathway. [ABSTRACT FROM AUTHOR]

Ferroptosis is a novel form of programmed cell death that relies on the accumulation of intracellular iron ions, causing irreversible damage to cell membranes through extensive lipid peroxidation, ultimately leading to cell death. Ferroptosis is closely associated with various neurodegenerative diseases. The ferroptosis of glial cells can regulate neuronal death by inducing neuroinflammation and affecting oxidative stress, thereby exacerbating the progression of neurodegenerative diseases. This review summarizes how ferroptosis occurs in different types of glial cells and its impact on neurons, aiming to deeply understand the effects of glial cell ferroptosis on neurodegenerative diseases and explore the potential therapeutic applications of inhibiting this process in treatment. [ABSTRACT FROM AUTHOR]

Objective To investigate the protective effect and mechanism of ginsenoside Rg1 (G-Rg1) on interleukin6 (IL-6) -induced neuronal injury in rats by regulating Janus activated kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Methods After culture, rat hippocampal neurons were divided into the control group (normal culture), the IL-6 model group (50 µg/L IL-6 was used to treat rat hippocampal neurons for 18 h to simulate the inflammatory environment in brain), the G-Rg1 low dose (10 µmol/L) group and the G-Rg1 high dose (40 µmol/L) group. After 48 h of normal culture, the survival rate of hippocampal neurons was determined by MTT method. The total iron load of neurons was detected by spectrophotometry, and levels of ferroptosis markers glutathione (GSH) and glutathione peroxidase 4 (GPX4) were detected. The mRNA expression level of ferroportin 1 (FPN1) in hippocampal neurons was detected by qRTPCR. The expression of proteins related to the neuronal JAK/STAT3 signaling pathway was detected by Western blot assay. Results Compared with the CON group, the neuronal survival rate, GSH content, GPX4 content and FPN1 mRNA expression level were decreased in the IL-6 model group, and the total iron load, p-JAK and p-STAT3 protein expression levels were increased (P＜0.05). Compared with the IL-6 model group, the neuronal survival rate, GSH content, GPX4 content and FPN1 mRNA expression level were increased in the low-dose and high-dose G-Rg1 groups, and the total iron load, p-JAK and p-STAT3 protein expression levels were decreased (P＜0.05). Changes of the above indicators were more significant in the high-dose G-Rg1 group than those in the low-dose G-Rg1 group (P＜0.05). Conclusion The mechanism of G-Rg1 alleviating ferroptosis of hippocampal neurons in rats may be related to the inhibition of IL-6/JAK/STAT3 signaling pathway, up-regulation of FPN1 expression, and prevention of iron overload. [ABSTRACT FROM AUTHOR]

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AIM: To investigate the mechanism by which Qiangji decoction attenuates cognitive impairment and mitochondrial dysfunction induced by D-galactose. METHODS: Eighty C57BL/6 mice were randomly divided into control group, model group, metformin group, and Qiangji decoction group. D-galactose （100 mg·kg-1·d-1） was injected into the neck of mice, excluding those in control group, for 8 weeks to establish an aging-related cognitive impairment model. The mice in Qiangji decoction group received Qiangji decoction （24. 96 g·kg-1·d-1）, those in metformin group received metformin （0. 2 g·kg-1·d-1）, and those in other groups were administered an equal volume of normal saline for 4 weeks （20 mL·kg-1·d-1）. Morris water maze and novel object recognition tests were used to assess mouse learning and memory. Fluoro-Jade B （FJB） staining was used to observe damaged neurons in the hippocampus. Transmission electron microscopy was employed to observe the ultrastructure of mitochondria in hippocampal nerve cells. The levels of reactive oxygen species （ROS） in hippocampal nerve cells were detected using a kit. Mitochondrial membrane potential was measured by JC-1 staining. Kits were used to measure the levels of mitochondrial ATP, and mitochondrial respiratory chain complexes I, III and IV in the hippocampus. The protein levels of AMP-activated protein kinase α（ AMPKα）, phosphorylated AMPKα at Thr172 （p-AMPKα-Thr172）, silent information regulator 1 （SIRT1）, peroxisome proliferator-activated receptor γ coactivator-1α （PGC-1α）, nuclear respiratory factor 1 （NRF1）, NRF2 and mitochondrial transcription factor A （TFAM） in the hippocampus were detected by Western blot. RESULTS: Morris water maze and novel object recognition tests showed that compared with model group, the escape latency of the mice in metformin and Qiangji decoction groups significantly decreased （P<0. 05 or P<0. 01）, while the number of platform crossings, time spent in the target quadrant, and novel recognition index significantly increased （P<0. 05 or P<0. 01）. The results of FJB staining indicated that compared with model group, the numbers of FJB-positive neurons in mouse hippocampal CA1 and CA3 regions significantly decreased in metformin and Qiangji decoction groups （P<0. 05 or P<0. 01）. Transmission electron microscopy revealed that compared with model group, damaged mitochondria in mouse hippocampal neurons were reduced in metformin and Qiangji decoction groups, with increased mitochondrial length and area （P<0. 05 or P<0. 01）. Compared with model group, ROS levels in mouse hippocampal neurons significantly decreased in metformin and Qiangji decoction groups （P< 0. 05 or P<0. 01）. The results of JC-1 staining demonstrated that compared with model group, mitochondrial membrane potential significantly increased in metformin and Qiangji decoction groups （P<0. 05 or P<0. 01）. Compared with model group, the levels of mitochondrial ATP, and complexes I, III and IV in the hippocampus significantly increased in metformin and Qiangji decoction groups （P<0. 05 or P<0. 01）. Western blot analysis showed that compared with model group, the protein levels of p-AMPKα-Thr172, SIRT1, PGC-1α, NRF1, NRF2 and TFAM in mouse hippocampal tissues significantly increased in metformin and Qiangji decoction groups （P<0. 05 or P<0. 01）. CONCLUSION: Qiangji decoction alleviates cognitive impairment, neuronal damage and mitochondrial dysfunction induced by D-galactose through activation of the AMPKα/SIRT1/PGC-1α signaling pathway. [ABSTRACT FROM AUTHOR]

CPG makes a great contribution to the control of gait motions in hexapod robots. To manage the gait movements of hexapod robots more efficiently and with lower energy consumption, this work introduced a Spiking-CPG(SCPG) neural network as the bionic control system for these robots. The system integrated Hopf oscillators with biologically inspired LIF neurons, which communicated through sparse spiking signals, in a ring topology. It was composed of six groups, each containing 2 000 LIF neurons, interconnected to form the network. This SCPG control system could produce common hexapod robot gaits such as the wave, tetrapod, and tripod gaits. It facilitated rapid, smooth, and stable transitions between motion gaits by adjusting phase difference parameters, and could dynamically adjust the required frequency and amplitude, exhibiting excellent robustness by quickly recovering from external disturbances. It controlled a simple 3D hexapod robot model on the Webots platform. It developed the robot by transforming the SCPG signal output through joint mapping functions, validating the motion stability of the designed hexapod robot and the feasibility and effectiveness of the SCPG control scheme. Finally, it ported the SCPG neural network controller proposed to Intel's Loihi chip, showing that it has high execution speed and lower energy consumption, indicating a promising prospect for application in the motion control of hexapod robots. [ABSTRACT FROM AUTHOR]

Copyright of Control Theory & Applications / Kongzhi Lilun Yu Yinyong is the property of Editorial Department of Control Theory & Applications and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

OBJECTIVE: To probe into the effects of high-frequency repetitive transcranial magnetic stimulation (rTMS) assisted by edaravone and camphor on neuronal protection, oxidative stress and cognitive function Improvement in patients with mild cognitive impairment (MCI). METHODS: Totally 100 patients with MCI admitted into Hebei Cangzhou Hospital of Integrated Chinese and Western Medicine from Mar. 2022 to Apr. 2023 were extracted to be divided into the observation group and control group via the lottery method, with 50 cases in each group. The control group received high-frequency rTMS treatment, while the observation group was given adjuvant treatment with edaravone and camphor on the basis of the control group. The therapeutic efficacy and adverse drug reactions of two groups were observed, and the Neurological Function Scale (NIHSS), Simplified Mental State Evaluation Scale ( MMSE), and Montreal Cognitive Assessment Scale ( MoCA) scores and serum levels of malondialdehyde (MDA), myeloperoxidase (MPO), superoxide dismutase (SOD), neuron specific enolase (NSE), plasma brain natriuretic peptide (BNP), and C-reactive protein (CRP) of two groups were compared. RESULTS: The total effective rate of observation group was 94. 00% (47/50), significantly higher than that 78. 00% (39/50) of control group, the difference was statistically significant (P<0. 05). After treatment, the MMSE and MoCA scores of both groups increased, and the observation group was higher than the control group, with statistically significant differences (P<0. 05). After treatment, the NIHSS scores of both groups decreased, and the observation group was lower than the control group, with statistically significant differences (P<0. 05). After treatment, MDA, NSE, BNP, CRP, MPO in the observation group were lower than those in the control group and before treatment, while SOD was higher than those in the control group and before treatment, with statistically significant differences (P<0. 05). The incidence of adverse drug reactions in observation group and control group was respectively 10. 00% (5/50) and 4. 00% (2/50), with no statistically significant difference (P>0. 05). CONCLUSIONS: rTMS assisted by edaravone and camphor in the treatment of patients with MCI can significantly improve cognitive function, promote neuronal repair, alleviate oxidative stress response, and improve clinical efficacy. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Sichuan University (Medical Science Edition) is the property of Editorial Board of Journal of Sichuan University (Medical Sciences) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the protective effect of dihydromyricetin (DMY) against injury of primary hip-pocampal neurons caused by ferric ammonium citrate (FAC) and its mechanism. Methods Primary hippocampal neurons were collected from 24-hour neonatal Sprague-Dawley rats for in vitro culture, and CCK-8 assay was used to measure the viability of primary hippocampal neurons treated with different concentrations of DMY and determine the administration concentration of DMY. Primary hippocampal neurons were divided into control group (H group), 100 mmol/L DMY treatment group (I group), 250 mmol/L FAC treatment group (J group), and 100 mmol/L DMY+250 mmol/L FAC treatment group (K group). Flow cytometry was used to measure the content of reactive oxygen species (ROS) in each group; colorimetry was used to measure the content of malondialdehyde (MDA) in each group; Western blot was used to measure the protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and glutathione peroxidase 4 (GPX4) in each group. Results CCK-8 assay showed the highest viability of primary hippocampal neurons at the concentration of 100 mmol/L for DMY (F=9.95,P

Objective To investigate the protective effect of 4-hydroxymandelic acid (4-HMA) against neuronal cell injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R) and brain tissue damage induced by middle cerebral artery occlusion/reperfusion (MCAO/R) in mice and its mechanism. Methods Primary neuronal cells were extracted and divided into control group (cultured in neuronal culture medium), OGD/R group (treated with OGD/R), and OGD/R+4-HMA group (treated with OGD/R and 4-HMA intervention). After 6 h of cells culture, Western blot was used to measure the levels of protein kinase B (Akt) and phosphorylated Akt (p-Akt) in neuronal cells of each group, and CCK-8 assay was used to measure cell viability in each group. C57BL/6 mice were randomly divided into Sham group, MCAO/R group, and MCAO/R+4-HMA group, with 6 mice in each group. The mice in the Sham group were given an external carotid artery stoma alone, but without middle cerebral artery occlusion. The mice in the MCAO/R group and the MCAO/R+4-HMA group were given MCAO surgery, with the restoration of blood flow after middle cerebral artery occlusion for 1.5 h; the mice in the MCAO/R+4-HMA group were given intraperitoneal injection of 4-HMA at 0 and 3 h after the restoration of blood flow, while those in the MCAO/R group were not given such treatment. TTC staining was used to measure the percentage of cerebral infarct volume and calculate the percentage of infarct area in total brain volume, and modified Neurological Severity Score (mNSS) was used to assess the behaviors of mice. Results Compared with the control group, the OGD/R group and the OGD/R+4-HMA group had significant increases in the re-lative expression level of p-Akt and p-Akt/Akt ratio (F=10.49,8.87,tLSD=3.02-3.14,P0.05). The OGD/R+4-HMA group had a significantly higher cell viability than the OGD/R group (F=104.60,tLSD=7.28,P

Copyright of Journal of Chinese Institute of Food Science & Technology / Zhongguo Shipin Xuebao is the property of Journal of Chinese Institute of Food Science & Technology Periodical Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Wool Textile Journal is the property of National Wool Textile Science & Technology Information Center and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To observe the ameliorating effect of intragastric administration of Klotho protein on cerebral ischemia-reperfusion injury (CIRI) in rats with acute cerebral infarction (ACI) and to explore its mechanism. Methods Fifty SD male rats were divided into the sham operation group, model group, low-dose Klotho group, medium-dose Klotho group and high-dose Klotho group, with 10 rats in each group. CIRI models after ACI were established in the model group, low-dose Klotho group, medium-dose Klotho group and high-dose Klotho group. In the sham operation group, only carotid artery vessel separation and wound suture were performed, and carotid artery clamping was not performed. After being fed for 24 h, the rats in the low-dose, medium-dose and high-dose Klotho groups were treated with 25，50 and 100 mg/kg Klotho protein, respectively, and the rats in the model group and sham operation group were treated with equal volume of normal saline. All rats in the five groups were treated once a day, for 14 days. Longa scoring method and balance beam scoring method were used to evaluate the neurological scores of rats in each group. Cerebral tissues of rats in each group were taken after decapitation. Hematoxylin staining method was used to measure the apoptosis rate of cerebral cortex neurons of rats, and receptor-interacting protein kinase 1（RIP1) and RIP3 proteins in cerebral cortex tissues of rats were detected by Western blotting. The inflammatory mediators interleukin (IL) -1β, tumor necrosis factor (TNF) -α and IL-6 were detected by enzyme-linked immunoassay, MDA was detected by TBA, SOD was detected by enzyme-linked immunoassay, and GSH-Px was detected by ultraviolet colorimetry. Results The the neurological score and cerebral cortical neuron apoptosis rate of rats in the sham operation group were lower than those in the other groups (all P<0. 05), and those in the model group were higher than those in the other groups (all P<0. 05), and those in the high-dose Klotho group were higher than those in the low-dose Klotho group and medium-dose Klotho group (all P<0. 05), and those in the mediumdose Klotho group were higher than those in the low-dose Klotho group (all P<0. 05) . The relative expression levels of RIP1 and RIP3 proteins and the expression levels of IL-1β, TNF-α, IL-6 and MDA in the cerebral cortex of rats in the sham operation group were lower than those in the other groups, while the expression levels of SOD and GSH-Px were higher than those in the other groups (all P<0. 05) . The relative expression levels of RIP1 and RIP3 proteins and the expression levels of IL-1β, TNF-α, IL-6 and MDA in cerebral cortex of rats in the model group were higher than those in the other groups, while the expression levels of SOD and GSH-Px were lower than those in the other groups (all P<0. 05) . The relative expression levels of RIP1 and RIP3 proteins and the expression levels of IL-1β, TNF-α, IL-6 and MDA in the cerebral cortex of rats in the high-dose Klotho group were lower than those in the low-dose Klotho group and medium-dose Klotho group, while the expression levels of SOD and GSH-Px were higher than those of the low-dose and medium-dose Klotho groups (all P<0. 05) . The relative expression levels of RIP1 and RIP3 protein and the expression levels of IL-1β, TNF-α, IL-6 and MDA in cerebral cortex of rats in the medium-dose Klotho group were lower than those in the low-dose Klotho group, while the expression levels of SOD and GSH-Px were higher than those in the low-dose Klotho group (all P< 0. 05) . Conclusion Gastric administration of 100 mg/kg Klotho protein can alleviate CIRI in ACI rats, and its mechanism may be related to inhibiting the expression of RIP1 and RIP3 proteins in cerebral cortex and inhibiting the inflammatory response and oxidative stress response at the site of brain injury. [ABSTRACT FROM AUTHOR]

BACKGROUND: Long non-coding RNAs (lncRNAs), as important regulators of the inflammatory response, are involved in the immune-inflammation-brain crosstalk mechanism after ischemic stroke and have the potential to become a therapeutic agent for neurological dysfunction after ischemic stroke. OBJECTIVE: To analyze and summarize the molecular mechanism of lncRNA acting on glial cells involved in the neuroimmuno-inflammatory cascade response after ischemic stroke and the associated signaling pathways, pointing out that lncRNAs have the potential to regulate inflammation after ischemic stroke. METHODS: PubMed was searched using the search terms of “ischemic stroke, long non-coding RNA, neuroinflammation, immune function, signal pathway, microglia, astrocytes, oligodendrocyte, mechanism,” and 63 relevant documents were finally included for review. RESULTS AND CONCLUSION: In the early stage of ischemic stroke, the death of nerve cells due to ischemia and hypoxia activates the innate immune response of the brain, promoting the secretion of inflammatory factors and inducing blood-brain barrier damage and a series of inflammatory cascades responses. As an important pathogenesis factor in ischemic stroke, the neuroimmuno-inflammatory cascade has been proved to seriously affect the prognosis of patients with ischemic stroke, and it needs to be suppressed promptly in the early stage. Neuroinflammation after ischemic stroke usually induces abnormal expression of a large number of lncRNAs that mediate a series of neuro-immune-inflammatory crosstalk mechanisms through regulating the polarization of microglia, astrocytes and oligodendrocytes to exert post-stroke neuroprotective effects. LncRNAs, as important regulatory factors of the inflammatory response, inhibit the neuroimmuno-inflammatory cascade response after ischemic stroke through regulating nuclear factor-κB, lncRNA-miRNA-mRNA axis, Rho-ROCK, MAPK, AKT, ERK and other signaling pathways to effectively improve neurological impairment after ischemic stroke. Most of experimental studies on the interaction between lncRNAs and ischemic stroke are based on a middle cerebral artery occlusion model or a cerebral ischemia-reperfusion injury model, but no clinical trials have been conducted. Therefore, it remains to be further explored about whether lncRNAs can be safely applied in clinical practice. At present, there are many therapeutic drugs for the treatment of ischemic stroke, but there are relatively few studies on the application of lncRNAs, exosomes and other transplantation technologies for the treatment of ischemic stroke using tissue engineering technology, which need to be further explored. lncRNA has become an important target for the treatment of ischemic stroke with its relative stability and high specificity. In future studies, more types of inflammatory lncRNAs that function under ischemic-hypoxia conditions should continue to be explored, in order to provide new research directions for the treatment of neuroinflammation after ischemic stroke. [ABSTRACT FROM AUTHOR]

As resident immune cells of central nervous system （CNS）， microglia play a key role in immune surveillance and tissue repair. They can be activated by various types of pathological factors to form M1 or M2 phenotype， which mediates neuroinflam-mation or neuroprotective effects. At the same time， when the homeostasis of the microenvironment in which the neuron is located is broken， "signal" molecules are also released to induce microglial activation through ligand-receptor binding. Therefore， the regulation of microglia-neuron connection is of great significance for treatment of nervous system diseases. This article reviews the signaling mole-cules involved in the two-way interaction between microglial cells and neurons， and elucidates the immune mechanisms of microglianeuron， thus providing a basis for targeted treatment of CNS diseases related to microglia activation. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Jilin University (Science Edition) / Jilin Daxue Xuebao (Lixue Ban) is the property of Zhongguo Xue shu qi Kan (Guang Pan Ban) Dian zi Za zhi She and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Jilin University (Science Edition) / Jilin Daxue Xuebao (Lixue Ban) is the property of Zhongguo Xue shu qi Kan (Guang Pan Ban) Dian zi Za zhi She and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the changes of retinal nerve fiber layer (RNFL) thickness and superficial vascular density in patients with Parkinson's disease (PD), and analyze the correlation between the changes and disease severity. Methods Total 43 patients (76 eyes) with PD admitted to the Affiliated Hospital of North Sichuan Medical College from June 2021 to March 2022, and 45 patients (90 eyes) with normal neurological and visual functions from their family members were recruited as the control group. Optical coherence tomography angiography (OCTA) was used to measure RNFL thickness, retinal blood vessel length density and perfusion density, and the area and circumference of foveal avascular zone (FAZ). Disease severity was evaluated by modified Hoehn - Yahr staging, and motor function was evaluated by Unified Parkinson's Disease Rating Scale III (UPDRS III) in PD group. Pearson and partial correlation analyses were used to investigate the correlation between retinal parameters and PD severity. Results Comparison of OCTA related parameters between the 2 groups: RNFL thickness (t = - 6.424, P = 0.000), central length density (t = - 3.629, P = 0.000), inner ring length density (Z = - 2.846, P = 0.004) and central perfusion density (Z = - 2.703, P = 0.007) in the PD group were lower than those in the control group. Correlation analysis showed that RNFL thickness was negatively correlated with UPDRS-III score (r = - 0.625, P = 0.000). Conclusions RNFL thickness may be a potential indicator for early diagnosis and evaluation of the severity of PD. [ABSTRACT FROM AUTHOR]

IM: To explore the mechanism by which Chaijin-Jieyu-Anshen tablet (CJJY)-medicated serum prevents synaptic injury in rat anterior cingulate cortex (ACC) neurons using an in vitro depression model. METHODS: Cells (astrocytes, microglia and neurons) were isolated from the ACC of SD rats. The isolated cells were characterized by immunofluorescence staining. An in vitro depression model was developed using 1 mg/L lipopolysaccharide (LPS) combined with 200 imol/L corticosterone (CORT). These cells were divided into control group, model group (CORT+LPS), glucocorticoid receptor (GR) blocker (GR-) group (CORT+LPS+RU486), GR agonist (GR+) group (CORT+LPS+dexa-methasone), CX3C chemokine receptor 1 (CX3CR1) blocker (CX3-) group (CORT+LPS+AZD8797), CX3CR1 agonist (CX3+) group (CORT+LPS+fractalkine), CJJY group (CORT+LPS+CJJY-medicated serum), CJJY/GR+ group (CORT+ LPS+CJJY-medicated serum+dexamethasone), and CJJY/CX3+ group (CORT+LPS+CJJY-mediated serum+fractalkine). The morphological characteristics of all ACC cells were observed by high-content analysis. The levels of neuroendocrine-related factors, adrenocorticotropic hormone (ACTH), corticotropin-releasing hormone (CRH) and CORT, and neuroin-flammatory mediators, tumor necrosis factor-a (TNF-a ), interleukin-1 p (IL-1p), IL-6 and glutamate (Glu), in the cell supernatants were quantified by ELISA. Immunofluorescence staining was used to analyze the protein expression of GR and vesicular glutamate transporter 1 (VGluTl) in astrocytes, as well as CX3CR1 and adenosine A2A receptor (A2AR) in microglia. Immunofluorescence staining with Nissl and p -tubulin was performed to evaluate synaptic damage in ACC neurons. RESULTS: In an in vitro model of depression, CJJY-medicated serum prevented morphological damage to ACC neurons, microglia and astrocytes. Moreover, CJJY-medicated serum reversed abnormal increases in the levels of ACTH, CRH, CORT, TNF-a, IL-1p, IL-6 and Glu in cell supernatants (P<0. 05 or P<0. 01). It was also found that CJJY-medicated serum reduced abnormal expression of GR, VGluT1, CX3CR1 and A2AR (P<0. 05 or P<0. 01), alleviating damage to the neuronal dendrites and dendritic spines of ACC neurons. CONCLUSION: The CJJY-medicated serum regulates GR/CX3CR1 double signaling in glia, and attenuates rat ACC neuronal synaptic damage in an in vitro depression model, indicating that CJJY-medicated serum controls depression by affecting the GR/CX3CR1 double signaling. [ABSTRACT FROM AUTHOR]

Deltamethrin (DM) has been widely used as a type II pyrethroid insecticide. Its high lipophilicity allows it to easily pass through the blood-brain barrier and affect the nervous system. However, its impact on the early neural development of zebrafish and the mechanism of toxicity remains unclear. In this study, zebrafish (Danio rerio) embryos were exposed to DM with different concentration of 0,10, 20 and 50 µg⋅L-1 to analyze the development and movement ability. The neurotoxicity of DM to zebrafish larvae was evaluated on the development of the nerve cells of transgenic zebrafish line. The results showed that the frequency of spontaneous coiling decreased 41.2% (P<0.001) by 50 µg⋅L-1 DM exposure at 24 hpf. The hatching rate of all the DM exposure groups was higher than the control group and heart rate were significantly increased in 20 and 50 µg⋅L-1 groups (P<0.01, P< 0.0001), and the body length was significantly reduced (P<0.01) at 36 hpf. These results showed that the effect of DM on embryo development was dose-dependent. Through the analysis of the spontaneous swim, light-dark stimulus and open field behavior of zebrafish larvae, it was found that zebrafish larvae became sluggish in those three scenarios, indicating that DM exposure affected the mobility of zebrafish, and the ability to respond to external environmental stimuli and the ability to actively explore new environments was weakened. Further analysis of transgenic zebrafish strains with specific markers for neural cell systems found that DM exposure caused a significant decrease in the number of nerve stem/progenitor cells in zebrafish (P<0.01, P<0.001), neuronal cell activity was enhanced, and the number of apoptotic cells was significantly increased (P<0.0001). The results suggested that the neurotoxicity of zebrafish larvae induced by DM is related to the nerve cell viability. DM is toxic to the central nervous system of zebrafish by destroying the number of nerve stem / progenitor cells, over-activating neurons and promoting apoptosis of nerve cells, thus affecting the behavior of zebrafish embryos and larvae. [ABSTRACT FROM AUTHOR]

Objective To analyze the clinical characteristics of anti - neuronal antibody positive paraneoplastic neurological syndrome related to immune checkpoint inhibitors (ICI - PNS). Methods and Results A total of 5 patients with anti - neuronal antibody positive ICI - PNS in Peking Union Medical College Hospital from January 2012 to March 2024 were included. Tumor types included small cell lung cancer (2 cases), malignant melanoma (one case), Hodgkin lymphoma (one case) and cervical cancer (one case). Immune checkpoint inhibitors (ICIs) included programmed death 1 (PD - 1) inhibitors (3 cases), programmed cell death ligand 1 (PD-L1) inhibitors (one case) and bispecific PD-1/cytotoxic T lymphocyte- associated antigen 4 (CTLA -4) inhibitors (one case). All 5 patients presented with high -risk neurologic phenotypes of paraneoplastic neurological syndrome (PNS), of which 4 presented with limbic encephalitis and one presented with rapidly progressive cerebellar syndrome. Anti - neuronal antibodies detected in serum and/or cerebrospinal fluid of patients included anti - Hu, γ - aminobutyric acid receptor type B (GABABR), sex-determining region of Y chromosome-related high mobility group box 1 (SOX1), metabotropic glutamate receptor 5 (mGluR5) and Yo antibodies. Neurological syndromes occurred within 2 weeks after receiving ICIs in 4 patients. The modified Rankin Score (mRS) of 4 patients was 3 at peak of illness, and one patient was 5 at peak of illness. The Common Terminology Criteria for Adverse Events (CTCAE) was grade 3 in all 5 patients. After withdrawal of ICIs and treatment with glucocorticoids and intravenous immunoglobulin (IVIg), the neurological symptoms of the patients were improved. Conclusions High/ intermediate - risk anti - neuronal antibodies are diagnostic markers of ICI - PNS. Evaluation of ICI - PNS clinical phenotypes and CTCAE grading are important for immunotherapy. Discontinuation of ICIs, administration of glucocorticoids and IVIg can improve the prognosis of patients.

Convolutional Neural Network (CNN) is widely used for image target classifications in Synthetic Aperture Radar (SAR), but the lack of mechanism transparency prevents it from meeting the practical application requirements, such as high reliability and trustworthiness. The Class Activation Mapping (CAM) method is often used to visualize the decision region of the CNN model. However, existing methods are primarily based on either channel-level or space-level class activation weights, and their research progress is still in its infancy regarding more complex SAR image datasets. Based on this, this paper proposes a CNN model visualization method for SAR images, considering the feature extraction ability of neurons and their current network decisions. Initially, neuronal activation values are used to visualize the capability of neurons to learn a target structure in its corresponding receptive field. Further, a novel CAM-based method combined with channel-wise and spatial-wise weights is proposed, which can provide the foundation for the decision-making process of the trained CNN models by detecting the crucial areas in SAR images. Experimental results showed that this method provides interpretability analysis of the model under different settings and effectively expands the application of CNNs for SAR image visualization.

Objective To investigate the effect of proanthocyanidins (PC) on the neurite outgrowth of rat dorsal root ganglion (DRG) neurons. Methods In vitro, primary rat DRG neurons were cultured with a series of concentration of PC to assess the effect of PC on the number and length of neurites as well as the morphology of growth cone. In vivo, the expression of growth associated protein 43 (GAP43) in the early stage of injury was detected using the sciatic nerve crush model. Finally, the impact of PC on nerve growth factor (NG)) expression in DRG neurons was evaluated in vitro using immunofluorescence and ELISA. Results PC significantly increased the number and length of neurites and the number of pseudopodium in growth cones of DRG neurons. PC also promoted the expression of GAP43 in the early stage of sciatic nerve injury in rats and enhanced the expression of NGF in DRG neurons. Conclusion PC may promote the neurite outgrowth by increasing the expression of NGF in DRG neurons. [ABSTRACT FROM AUTHOR]

BACKGROUND: Inflammation is one of the important factors that induce cerebral ischemia-reperfusion injury. Studies have shown that electroacupuncture can effectively reduce inflammation after ischemic stroke and improve the symptoms of neurological deficits, but the mechanism is not clear. OBJECTIVE: To observe the effect of electroacupuncture on Toll-like receptor 4/nuclear factor-κB in rats with cerebral ischemia-reperfusion injury. METHODS: Forty-eight male Sprague-Dawley rats were randomly divided into sham operation group, model group and electroacupuncture group, with 16 rats in each group. The rat model of cerebral ischemia-reperfusion injury was prepared by middle cerebral artery occlusion. At 24 hours after modeling, the rats in the electroacupuncture group were treated with electroacupuncture, once a day, 20 minutes each time, for a total of 5 days. The sham operation group and the model group did not do any intervention. After 5 days of intervention, Longa method was used to evaluate the degree of neurological injury in rats. Triphenyl tetrazolium chloride staining and hematoxylin-eosin staining were used to measure the volume of cerebral infarction and the pathological changes of brain tissue in rats. Serum interleukin-6, interleukin-18 and tumor necrosis factor-α were detected by ELISA. Expressions of Toll-like receptor 4 and nuclear factor-κB in the cerebral cortex at mRNA and protein levels were detected by fluorescence quantitative PCR and western blot, respectively. RESULTS AND CONCLUSION: Compared with the sham operation group, the neurological function scores, serum interleukin-6, interleukin-18, and tumor necrosis factor-α levels, Toll-like receptor 4 and nuclear factor-κB mRNA and protein expression levels were significantly higher in the model group (P < 0.01). Compared with the model group, electroacupuncture significantly reduced the neurological function scores, serum interleukin-6, interleukin-18, and tumor necrosis factor-α levels, Toll-like receptor 4 and nuclear factor-κB mRNA and protein expression levels (P < 0.05, P < 0.01). Compared with the sham operation group, the volume of cerebral infarction in the model group increased significantly (P < 0.01). Compared with the model group, the volume of cerebral infarction in the electroacupuncture group decreased (P < 0.05). In the model group, the arrangement of neurons was disordered, some nerve cells disappeared, nuclei presented with pyknosis and incomplete structure. After electroacupuncture intervention, the degree of neuronal degeneration and neuronal loss in the cerebral cortex of rats were reduced compared with those in the model group. To conclude, electroacupuncture can significantly improve the neurobehavior of rats with cerebral ischemia-reperfusion injury, reduce brain tissue injury, and effectively reduce the level of serum inflammatory factors. The mechanism may be related to the inhibition of Toll-like receptor 4/nuclear factor-κB signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To explore the effects of astragaloside on neural dysfunction and neuronal apoptosis of traumatic brain injury (TBI) in rats through Fas/FasL signaling pathway. Methods Fifty rats were randomly divided into 5 groups: the sham operation group, the model group, the astragaloside group (20 mg/kg), the Fas silencing group [4 µg Fas small interfering RNA (siRNA) lentiviral vector] and the astragaloside+Fas silencing group (20 mg/kg astragaloside+4 µg Fas siRNA lentiviral vector). Each group consisted of 10 rats. Except the sham operation group, the other groups of rats were established TBI rat model. Each group was received medication intervention according to the corresponding dosage, once a day, for 7 days. Water maze test was used to detect the nerve function defect in rats. Fluorescence quantitative PCR was used to detect expression levels of Fas and FasL messenger RNA (mRNA) in brain tissue. Hematoxylin-eosin, β-tubulin III (Tuj1) immunofluorescence and TUNEL staining were used to observe pathological changes, neuronal activity and apoptosis of brain tissue, respectively. Western blot assay was used to detect expression levels of Fas/FasL pathway, Caspase-3, Bcl-2 associated X protein (Bax) and B lymphoblastoma-2 (Bcl-2) protein in brain tissue. Results Compared with the sham operation group, the cell gap was increased and degeneration was obvious in brain tissue in the model group. The escape latency of rats on days 1-5, neuronal apoptosis rate, Caspase-3, Bax protein, Fas, FasL mRNA and protein levels were increased (P＜0.05). The number of times crossing platforms, the number of Tuj1 positive cells and Bcl-2 protein were decreased (P＜0.05). Compared with the model group, in the astragaloside group and the Fas silencing group, the cell gap in brain tissue was narrowed and degeneration was reduced, the escape latency of rats on days 1-5, neuronal apoptosis rate, Caspase-3, Bax protein, Fas, FasL mRNA and protein levels were decreased, and the number of crossing platforms, the number of Tuj1 positive cells and Bcl-2 protein level were increased (P＜0.05). There were no significant differences in pathological changes of brain and the above indexes between the astragaloside group and the Fas silencing group (P＞0.05). Compared with the astragaloside group and the Fas silencing group, the pathological damage of brain tissue of rats was further reduced in the astragaloside+Fas silencing group, neuronal apoptosis rate, Caspase-3, Bax protein, Fas, FasL mRNA and protein levels were decreased, and the number of Tuj1 positive cells and Bcl-2 protein were increased (P＜0.05). Conclusion Astragaloside may reduce nerve function deficit and neuronal apoptosis in TBI rats by inhibiting Fas/FasL signaling pathway mediated apoptosis pathway. [ABSTRACT FROM AUTHOR]

To investigate the influence of Yiqi Shengqing recipe on neuronal pyroptosis in ischemic stroke rats by regulating hypoxia inducible factor-1α (HIF-1α)/NOD-like receptor thermal protein domain associated protein 3 (NLRP3) signal pathway. Methods SD rats were randomly divided into the sham operation group (S group), the model group (M group), the low, medium and high dose (3.465, 6.930 and 13.860 g/kg) Yiqi Shengqing recipe groups, and high)dose Yiqi Shengqing recipe+HIF-1α activator DMOG (13.860 g/kg Yiqi Shengqing recipe+40 mg/kg DMOG) group, 15 animals in each group. The stroke model was constructed by thread plug method. After successful modeling, neural function defects were evaluated including TTC staining for evaluating the volume of cerebral infarction, ELISA for detecting the serum interleukin (IL)-1β and IL-18 levels, HE staining for detecting pathological changes of ischemic cortex, TUNEL staining for detecting neuronal apoptosis and Western blot assay for detecting the expression of pyroprotein and HIF-1α/NLRP3 pathway protein. Results Compared with the S group, the neurological deficit score, infarct volume, IL-1β, IL-18 contents, apoptosis rate of nerve cells, GasderminD-N (GSDMD-N), Caspase-1, HIF-1α and NLRP3 protein levels were increased in the M group (P＜0.05). Compared with the M group, the neurological defect score, infarct volume, IL-1β, IL-18 contents, neuronal apoptosis rate, GSDMD-N, Caspase-1, HIF-1α and NLRP3 protein levels were decreased in the low, medium and high dose Yiqi Shengqing recipe groups (P＜0.05). DMOG attenuated the improvement effect of high-dose Yiqi Shengqing recipe on neuronal death in ischemic stroke rats. Conclusion Yiqi Shengqing recipe may reduce the neuronal pyroptosis in ischemic stroke rats by down-regulating HIF-1α/NLRP3 signal pathway. [ABSTRACT FROM AUTHOR]

BACKGROUND: Bone defects are caused by many factors, such as inflammation, tumor, trauma or bone diseases. Erythropoietin can promote the differentiation of mesenchymal stem cells into osteoblasts and osteoclasts and act on vascular endothelial cells to induce angiogenesis and accelerate the repair of bone and cartilage defects. Erythropoietin is a growth factor with potential application in bone tissue engineering construction. OBJECTIVE: To expound the application and potential mechanism of erythropoietin in bone tissue engineering. METHODS: The first author searched the related articles published in CNKI, WanFang, VIP, and PubMed databases from 2004 to 2022 by computer. Search terms were “erythropoietin, bone defect, bone regeneration, angiogenesis, osteogenesis, osteoblast, osteoclast, bone tissue engineering” in Chinese and English. Finally, 64 articles were included for review. RESULTS AND CONCLUSION: (1) Erythropoietin can directly act on osteoblasts and osteoclasts in the bone marrow microenvironment by promoting the differentiation of mesenchymal stem cells into osteoblasts, osteoclasts, adipocytes, nerve cells and stromal cells. The activation of Wnt/β-catenin, hypoxiainducible factor 1α/vascular endothelial growth factor, p38 MAPK and EphrinB2/EphB4 signaling pathways mediates the osteogenic differentiation of mesenchymal stem cells. (2) Erythropoietin can not only regulate the production of erythrocytes to alter the oxygen-carrying capacity of blood but also stimulate vascular endothelial cells to promote angiogenesis. The new blood vessels can carry oxygen, nutrients, growth factors, and bone progenitor cells necessary for osteogenesis to the osteogenic site, thereby promoting bone formation and fracture healing. (3) Currently, erythropoietin is being used as a growth factor with osteogenic and angiogenic effects in various types of scaffold materials such as chitosan, polycaprolactone, bioceramics, and nanofibers through various drug delivery methods. Erythropoietin, along with other growth factors such as bone morphogenetic protein-2 and bone morphogenetic protein-9, has been applied to the surface of scaffold materials to participate in the repair of bone defects. Erythropoietin has demonstrated excellent practicality in the construction of new tissue-engineered bone and has potential clinical application value. [ABSTRACT FROM AUTHOR]

BACKGROUND: Croton cream can activate ERK pathways and have anti-apoptotic effects on neuronal cells. It is not clear whether it synergistically exerts antiapoptotic effects by inhibiting the activation of JNK and p38 pathways. OBJECTIVE: To explore the effects and mechanisms of croton cream on neuronal damage and apoptosis in the ischemic cortex of rats with cerebral ischemiareperfusion injury. METHODS: (1) Ninety Sprague-Dawley rats were randomly divided into sham operation group, model group, croton cream low-dose group, croton cream medium-dose group, croton cream high-dose group and nimodipine group, with 15 rats in each group. Except for the sham operation group, animal models of middle cerebral artery occlusion were prepared in rats by the thread method. Rats in the three croton cream groups were given 20, 40, and 60 mg/kg croton cream, respectively. Rats in the sham operation and model groups were given the same amount of normal saline, once a day, for 7 consecutive days. The optimal concentration of croton cream, namely the high dose of croton cream, was selected based on neurological deficit score, TTC staining, brain tissue water content, hematoxylin-eosin staining and Nissl staining. (2) Another 120 Sprague-Dawley rats were randomly divided into sham operation group, model group, croton cream group, JNK inhibitor group, croton cream+JNK inhibitor group, p38 MAPK inhibitor group, croton cream+p38 MAPK inhibitor group, and nimodipine group, with 15 rats in each group. Animal models of middle cerebral artery occlusion were prepared using the thread method in all the groups except in the sham operation group. Thirty minutes before modeling, 10 μL of SP600125 (JNK inhibitor) and 10 μL of SB203580 (p38 MAPK inhibitor) were injected into the lateral ventricle of the rats, respectively. Rats in croton cream groups were intragastrically given 60 mg/kg croton cream. Seven days later, the JNK/p38 MAPK signaling pathway, apoptosis-related proteins and cell apoptosis were detected by western blot, TUNEL staining and flow cytometry, respectively. RESULTS AND CONCLUSION: (1) Compared with the sham operation group, neurological deficit score, cerebral water content, cerebral infarction volume and apoptosis rate were significantly increased in the model group (P < 0.05), where nerve cells showed scattered distribution. Compared with the model group, neurological deficit score, water content of brain tissue and cerebral infarction volume were significantly decreased in the croton cream medium-dose group, high-dose group and nimodipine group (P < 0.05), and the pathological morphology of nerve cells was significantly improved. (2) Compared with the JNK inhibitor group, p-JNK/JNK, p-p38/p38 and Bax expressions in rat brain tissue and the apoptotic rate were significantly decreased in the croton cream+inhibitor groups (P < 0.05), while the expression of and Bcl-2 was significantly increased (P < 0.05). To conclude, croton cream may inhibit the activation of JNK/p38 MAPK signaling pathway and reduce neuronal apoptosis to achieve neuroprotective effects in rats with cerebral ischemia-reperfusion injury. [ABSTRACT FROM AUTHOR]

Objective To analyze the influence of cyclic RNA homologous domain interacting protein kinase 3 (circ_HIPK3) on function and morphology of myloid β-protein (Aβ) induced hippocampal neurons by targeting miR-381-3p/ zinc finger protein 217 (ZNF217) axis. Methods Hippocampal neurons of neonatal rats were prepared and divided into the control group, the Aβ group, the si NC1 group, the si HIPK3 group, the si HIPK3+inhibitor NC group, the si HIPK3+miR381-3p inhibitor group, the si HIPK3+miR-381-3p inhibitor+si NC2 group and the si HIPK3+miR-381-3p inhibitor+si ZNF217 group. Except the control group, all the other groups were modeled by 40 µmol/L Aβ1~42. qRT-PCR was used to determine the circ of hippocampal neurons circ_HIPK3, miR-381-3p and ZNF217 mRNA levels. Cell morphology was observed by transmission electron microscope, and the survival rate of hippocampal neurons was measured by CCK-8 method. Hochesst 33342 method was used to measure apoptosis of hippocampal neurons. The intracellular Ca2+ fluorescence intensity of hippocampal neurons was detected by flow cytometry. The expression levels of P-Tau, B-cell lymphoma-2 (Bcl2), Bcl-2-associated X protein (Bax), Caspase-3 and ZNF217 proteins in hippocampal neurons were measured by Western blot assay. Double luciferase reporter genes were used to analyze the targeting relationship between miR-381-3p and circ_HIPK3, ZNF217. Results In the control group, the structure of hippocampal neurons was normal, the morphology of nucleus was normal, and there were no pathological changes in mitochondria and endoplasmic reticulum. In the Aβ group, hippocampal neurons showed degenerative changes, abnormal nuclear morphology, membrane invagination, a large number of mitochondria swelling and a large number of lipid droplets vacuoles in cytoplasm. Compared with the Aβ group, the hippocampal neuronal structure was partially restored in the si HIPK3 group. Compared with the si HIPK3 group, the hippocampal neuronal structure was severely damaged in the si HIPK3+miR-381-3p inhibitor group. Compared with the si HIPK3+miR-381-3p inhibitor group, the damage of hippocampal neurons in the si HIPK3+miR-381-3p inhibitor+si ZNF217 group was reduced. Compared with the control group, the circ_HIPK3, ZNF217 mRNA and ZNF217 protein levels, apoptosis rate, Ca2+ fluorescence intensity, P-Tau, Bax, Caspase-3 protein expression of hippocampal neurons were increased in the Aβ group, and the miR-381-3p level, survival rate and Bcl-2 protein expression decreased (P＜0.05). Compared with the Aβ group, the circ_HIPK3, ZNF217 mRNA and ZNF217 protein levels, apoptosis rate, Ca2+ fluorescence intensity, P-Tau, Bax and Caspase-3 protein expression of hippocampal neurons were decreased in the si HIPK3 group, and miR-381-3p level, survival rate and Bcl-2 protein expression increased (P＜0.05). Compared with the si HIPK3 group, the circ_HIPK3, ZNF217 mRNA and ZNF217 protein levels, apoptosis rate, Ca2+ fluorescence intensity, P-Tau, Bax and Caspase-3 protein expression of hippocampal neurons in the si HIPK3+miR-381-3p inhibitor group were increased, and the miR-381-3p level, survival rate and Bcl-2 protein expression decreased (P＜0.05). Compared with the si HIPK3+miR381-3p inhibitor group, the ZNF217 mRNA and ZNF217 protein levels, apoptosis rate, Ca2+ fluorescence intensity, P-Tau, Bax and Caspase-3 protein expression of hippocampal neurons in the si HIPK3+miR-381-3p inhibitor+si ZNF217 group were decreased, and the survival rate and Bcl-2 protein expression increased (P＜0.05). miR-381-3p targeted and combined with HIPK3 and ZNF217. Conclusion circ_HIPK3 silencing may ameliorate Aβ -induced damage of hippocampal neuronal structure and function by regulating miR-381-3p/ZNF217 axis. [ABSTRACT FROM AUTHOR]

The semi-supervised deep neural network modeling method has been widely applied in soft sensor, but the network based on hierarchical training only excavates the effective information of each input layer in the feature extraction process, ignoring the loss of effective information of the original input and accumulating it layer by layer, resulting in low accuracy of feature representation of the original input. In addition, the lack of spatiotemporal information related to the mining process can also lead to model performance degradation. This paper proposed a semi-supervised dynamics deep fusion neural network (SS- DDFNN) method. This method reconstructed the original input data and predicted quality variables at each layer of the feature extraction network. By using the reconstructed original input error in pre-training loss, it reduced the loss of effective information from the original input. Simultaneously it incorporated attention mechanism and t-distribution random neighborhood embedding to extract spatiotemporal related information, and established a gated neural network quality prediction model using extracted features. The experimental results show that compared to the SAE, GSTAE, and SIAE models, the proposed method has improved prediction accuracy by 2.8%, 1.1%, and 0.9% in the case of a debutanizer, respectively. In the industrial polyethylene production case, it has increased by 2.7%, 1.0%, and 0.7% respectively. The experimental results show that the pro- posed method is effective. [ABSTRACT FROM AUTHOR]

BACKGROUND: Animal models of diabetic encephalopathy that have been studied mainly include streptozotocin-induced model, high-sugar and high-fat dietinduced model and spontaneous animal model. Establishing a simple, easy, short-cycle, safe and effective model of diabetic encephalopathy can help to explore the subsequent pathogenesis and screen therapeutic drugs. OBJECTIVE: To further explore and evaluate the method of building diabetic encephalopathy rat models. METHODS: Twenty Sprague-Dawley rats were randomly divided into control (n=10) and model (n=10) groups. Rats in the model group were given a single injection of 45 mg/kg streptozotocin in the left lower abdominal cavity, and those in the control group were given the same amount of citrate buffer. During the experiment, the body mass, feed intake, water intake and blood glucose were measured. After 8 weeks, the glucose tolerance and oxidative stress levels were measured, and the pathological changes of brain tissue and the expression of apoptotic proteins were compared between groups. RESULTS AND CONCLUSION: Compared with the control group, the food intake, water intake, encephalization quotient, blood glucose and area under the blood glucose curve were significantly increased in the model group, while the body mass decreased significantly (P < 0.01). Histopathological examination of the brain showed that compared with the control group, the number of surviving nerve cells was significantly reduced in the model group (P < 0.01), with more significant pathological damage of nerve cells. Compared with the control group, the activities of serum superoxide dismutase, catalase and glutathione in the model group were significantly decreased (P < 0.01), and the content of oxidative malondialdehyde was significantly increased (P < 0.05). The expression levels of apoptosis-related proteins Bax and Caspase-3 in brain tissue increased in the model group compared with the control group, while the expression of Bcl-2 decreased (P < 0.01). In conclusion, an 8-week injection of 45 mg/kg streptozotocin can cause obvious pathological damage to the brain tissue of diabetic rats, to successfully establish the rat model of diabetic encephalopathy. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of astragaloside IV on cerebral tissue injury caused by ischemia/reperfusion (I/R) and pyroptosis mediated by Caspase-1 signaling pathway. Methods: SD rats were randomly divided into 4 groups of sham operation (Sham), model (MCAO/R), solvent control (DMSO) and astragaloside IV (AS IV). Cerebral I/R injury model was established by occlusion of the middle cerebral artery for 2 hours and reperfusion for 24 hours. Zea Longa score was used to observe the neurological deficit of rats, the volume of cerebral infarction in rats was evaluate by TTC staining, pathological changes of brain tissue was observed by HE staining, pyroptosis of brain was observed by Caspase-1 and TUNEL immunofluorescence double staining, and protein expressions of NLRP3, Cleaved Caspase-1, IL-18 and IL-1β in brain tissue were detected by Western blot. Results: By constructing the MCAO/R model, our findings suggest that astragaloside IV can reduce the neurological deficit caused by I/R in rats, reduce the infarct volume ofbrain, relieve the necrosis and loss of nerve cells on the infarct side, and inhibit pyroptosis by regulating the classical pyroptosis pathway mediated by Caspase-1. Conclusion: Astragaloside IV may alleviate cerebral I/R injury by inhibiting pyroptosis via regulating the classical pyroptosis pathway mediated by Caspase-1. [ABSTRACT FROM AUTHOR]

BACKGROUND: Endogenous neurogenesis and exogenous stem cell transplantation in the brain show great therapeutic potential for neurological diseases including ischemic stroke, repairing and replacing lost neurons, promoting synaptic remodeling, and inhibiting apoptosis. Traditional Chinese medicine and compound therapy for supplementing qi, activating blood circulation and inducing resuscitation for the treatment of neurological dysfunction after ischemia have certain advantages, targeting nerve repair through a variety of ways, including promoting endogenous neurogenesis and exogenous stem cell survival, proliferation, homing, and inducing neuronal differentiation. OBJECTIVE: To summarize the mechanism of traditional Chinese medicine and compound for supplementing qi, activating blood circulation and inducing resuscitation to promote nerve repair in the acute phase of ischemic stroke, in order to provide a reference for the research and treatment of new drugs in ischemic stroke. METHODS: The articles from CNKI and PubMed databases about traditional Chinese medicine and compound for supplementing qi, activating blood circulation and inducing resuscitation in promotion of nerve repair in the acute phase of ischemic stroke from 2010 to 2022 were searched, with “supplementing qi and activating blood circulation; inducing resuscitation; traditional Chinese medicine (TCM); compounds; ischemic stroke; nerve repair; stem cells” as Chinese and English search terms. After excluding old and duplicate views, the retrieved literature was analyzed and collated, and a total of 124 articles were included for analysis. RESULTS AND CONCLUSION: (1) The definition of stem cells, ischemic stroke and the nerve repair pathway in the acute phase of ischemic stroke were sorted out. (2) The mechanism of action of traditional Chinese medicine and compound for supplementing qi, activating blood circulation and inducing resuscitation to promote nerve repair in the acute phase of ischemic stroke was summarized, mainly including promoting stem cell proliferation, improving stem cell viability and survival rate, promoting nerve cell homing, inducing stem cell differentiation to neurons, inhibiting apoptosis of nerve cells, promoting axon regeneration, regulating angiogenesis and remodeling, improving the level of neurotrophic factors and repairing the integrity of the blood-brain barrier. (3) Through the existing research, the relevant factors and signaling pathways of traditional Chinese medicines and compounds for supplementing qi, activating blood circulation and inducing resuscitation to promote nerve repair in the acute phase of ischemic stroke were summarized, such as Nestin protein expression, DCX protein expression, brain-derived neurotrophic factor, vascular endothelial growth factor and Wnt/β-catenin signaling pathway, Notch signaling pathway, PI3k/ Akt signaling pathway, BDNF/TrkB signaling pathway and ERK/MAPK signaling pathway. It provides a relevant reference for future research on ischemic strokespecific drugs and new clinical treatment methods. [ABSTRACT FROM AUTHOR]

SNN has gained widespread attention due to its low power consumption and high-speed computing capabilities on neuromorphic chips. The conversion from DNN to SNN is an effective training method for SNN. However, there are approxima- tion errors in the conversion process, leading to significant performance degradation of the converted SNN under short time steps. Through a detailed analysis of the errors in the conversion process, this paper decomposed them into quantization and pruning errors and asymmetric errors, and proposed an improved adaptive threshold algorithm to balance the threshold of SNN. It used the mean square error(MMSE) to achieve a better balance between quantization and pruning errors. Additionally, this algorithm introduced a dual-threshold memory mechanism based on the IF neuron model to effectively address the asymmetric errors. Experimental results demonstrate that the improved algorithm achieves excellent performance on the CIFAR-10, CIFAR- 100 datasets, and the MIT-BIH arrhythmia dataset. For the CIFAR-10 dataset, it achieves a high accuracy of 93.22% with only. 16 time steps, validating the effectiveness of the algorithm. [ABSTRACT FROM AUTHOR]

Objective To investigate whether salvianolic acid B (Sal B) can improve the cognitive function in rats with post-traumatic stress disorder (PTSD) by regulating GSK-3β/β -Catenin signal pathway. Methods Sixty rats were randomly grouped into the normal group, the PTSD group, the Sal B low-dose group (10 mg/kg), the Sal B high-dose group (20 mg/kg) and the GSK-3β inhibitor group (30 mg/kg CHIR-99021), with 12 rats in each group. In addition to the normal group, rats in other groups were constructed PTSD rat models by using single prolonged stress (SPS) method. Open field test and Morris water maze test were applied to evaluate the cognitive function of rats. Nissl staining was applied to observe the pathological changes of hippocampal neurons. TUNEL staining was applied to detect the apoptosis of hippocampal neurons. Western blot assay was applied to detect the expression of cleared caspase-3, B-cell lymphoma gene-2-associated X protein (Bax), proto-oncogene (c-Myc), Cyclin D1, total GSK-3β (t-GSK-3β), phosphorylated GSK-3β (p-GSK-3β), total β-Catenin (t-β-Catenin) and phosphorylated β-catenin (p-β-Catenin) proteins in hippocampus. Results Compared with the PTSD group, the number of crawling spaces, standing times, total movement distance and times of crossing the original platform of rats were higher in the Sal B low-dose group, the Sal B high-dose group and the GSK-3β inhibitor group. The escape latency and the time to cross the original platform for the first time were shorter, the apoptosis rate of hippocampal neurons and the expression levels of Bax, cleaved caspase-3, t-GSK-3β and p-β-Catenin proteins in hippocampus were lower, and the expression levels of Cyclin D1, c-Myc, p-GSK-3β, t- β -Catenin proteins were higher (P＜0.05). Conclusion Sal B can reduce the apoptosis and damage of hippocampal neurons in rats with PTSD and improve cognitive dysfunction in rats, and inhibit the GSK-3β/β-Catenin signal pathway. [ABSTRACT FROM AUTHOR]