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Background: To comprehensively assess the neurologic recovery potential of chondroitinase ABC (ChABC) in rats after spinal cord injury (SCI)., Methods: The PubMed, Embase, ScienceDirect, Web of Science, and China National Knowledge Infrastructure databases were searched for animal experiments that evaluated the use of ChABC in the treatment of SCI up to November 2022. Studies reporting neurological function using the Basso, Beattie, and Bresnahan (BBB) scale, as well as assessments of cavity area, lesion area, and glial fibrillary acidic protein (GFAP) levels, were included in the analysis., Results: A total of 46 studies were ultimately selected for inclusion. The results of the study showed that rats with SCI that received ChABC therapy exhibited a significant improvement in locomotor function after 7 days compared with controls (32 studies, weighted mean difference (WMD) = 0.58, [0.33, 0.83], p  < 0.00001). Furthermore, the benefits of ChABC therapy were maintained for up to 28 days according to BBB scale. The lesion area was reduced by ChABC (5 studies, WMD = -20.94, [-28.42, -13.46], p  < 0.00001). Meanwhile, GFAP levels were reduced in the ChABC treatment group (8 studies, WMD = -29.15, [-41.57, -16.72], p <  0.00001). Cavity area is not statistically significant. The subgroup analysis recommended that a single injection of 10 μL (8 studies, WMD = 2.82, [1.99, 3.65], p <  0.00001) or 20 U/mL (4 studies, WMD = 2.21, [0.73, 3.70], p =  0.003) had a better effect on improving the function. The funnel plot of the BBB scale was found to be essentially symmetrical, indicating a low risk of publication bias., Conclusions: This systematic review and meta-analysis has indicated that ChABC could improve functional recovery in rats after SCI.

Context: Spinal cord injury (SCI) is a potentially fatal neurological disease with severe complications and a high disability rate. An increasing number of animal experimental studies support the therapeutic effect of quercetin, which is a natural anti-inflammatory and antioxidant bioflavonoid., Objective: This paper reviewed the therapeutic effect of quercetin on a rat SCI model and summarized the relevant mechanistic research., Data Sources: PubMed, EMBASE, Web of Science, Science Direct, WanFang Data, SinoMed databases, the China National Knowledge Infrastructure, and the Vip Journal Integration Platform were searched from their inception to April 2023 for animal experiments applying quercetin to treat SCI., Study Selection: Based on the PICOS criteria, a total of 18 eligible studies were included, of which 14 were high quality., Results: In this study, there was a gradual increase in effect based on the Basso, Beattie, and Bresnahan (BBB) score after three days ( p  < 0.0001). Furthermore, gender differences also appeared in the efficacy of quercetin; males performed better than females ( p  = 0.008). Quercetin was also associated with improved inclined plane test score ( p  = 0.008). In terms of biochemical indicators, meta-analysis showed that MDA ( p  < 0.0001) and MPO ( p  = 0.0002) were significantly reduced after quercetin administration compared with the control group, and SOD levels were increased ( p  = 0.004). Mechanistically, quercetin facilitates the inhibition of oxidative stress, inflammation, autophagy and apoptosis that occur after SCI., Conclusions: Generally, this systematic review suggests that quercetin has a neuroprotective effect on SCI.

Spinal cord injury (SCI) leads to loss of function below the lesion and affects individuals worldwide. An increasing number of experimental studies support the effectiveness of melatonin (MT) for SCI. Our objectives were to investigate neurological recovery and anti-oxidant effects of MT in animal models of SCI, and to explore the appropriate dose. Published MT studies in SCI animal models described in six databases were searched. Two practiced investigators selected the studies, extracted the data, and independently evaluated the quality of the included studies. A meta-analysis evaluated the effect of MT in SCI and a network meta-analysis was performed to explore the appropriate MT dose for SCI models. Thirteen studies were analyzed, of which three were high quality. The results of the meta-analysis manifested that the behavioral evaluation (Basso, Beattie, and Bresnahan scales, n = 90, p = 0.003; motor function scores, n = 92, p = 0.004; Tarlov's criteria, n = 150, p = 0.002; inclined plane test, n = 150, p = 0.001) and biochemical outcomes (malondialdehyde, n = 121, p = 0.0010; glutathione levels, n = 64, p < 0.0001; and myeloperoxidase activity, n = 32, p < 0.00001) were improved, compared with the control group, after MT administration. A dose of 12.5 mg/kg was most effective in SCI rat models. Studies indicated that MT administration significantly improved neurological recuperation and anti-oxidant effects in rat models of SCI. The appropriate dose of MT was 12.5 mg/kg for SCI rat models. The majority of included studies were low quality; however, optimal MT treatment in SCI still requires high quality studies.

Spinal cord injury (SCI) is a devastating condition affecting young, healthy individuals worldwide. Existing agents have inadequate therapeutic efficacy, and some are associated with side effects. Our objective is to summarize and critically assess the neurological recovery and antioxidant effects of curcumin for treatment of SCI in rat models. PubMed, Embase, and Chinese databases were searched from their inception date to February 2014. Two reviewers independently selected animal studies that evaluated neurological recovery and antioxidant effects of curcumin, compared to placebo, in rats with SCI, extracted data, and assessed the methodological quality. A pair-wise analysis and a network meta-analysis were performed. Eight studies with adequate randomization were selected and included in the systematic review. Two studies had a higher methodological quality. Overall, curcumin appears to significantly improve neurological function, as assessed using the Basso, Beattie, Bresnahan (BBB) locomotor rating scale (four studies, n=132; pooled mean difference [MD]=3.09; 95% confidence interval [CI], 3.40-4.45; p=0.04), in a random-effects model and decrease malondialdehyde (MDA) using a fixed-effects model (four studies, n=56; pooled MD=-1.00; 95% CI=-1.59 to -0.42; p=0.00008). Effect size, assessed using the BBB scale, increased gradually with increasing curcumin dosage. The difference between low- and high-dose curcumin using the BBB scale was statistically significant. Neurological recovery and antioxidant effects of curcumin were observed in rats with SCI despite poor study methodological quality.

Our study aimed to establish a model of compression injury of cervical dorsal root ganglia (DRG) in the rat and to investigate the pathological changes following compression injury and decompression procedures. Thirty rats were divided into three groups: control group receiving sham surgery, compression group undergoing surgery to place a micro-silica gel on C6 DRG, and decompression group with subsequent decompression procedure. The samples harvested from the different groups were examined with light microscopy, ultrastructural analysis, and horseradish peroxidase (HRP) retrograde tracing techniques. Apoptosis of DRG neurons was demonstrated with TUNEL staining. Changes in PGE2 and PLA2 in DRG neurons were detected with enzyme-linked immunosorbent assay (ELISA). Local expression of vascular endothelial growth factor (VEGF) was monitored with immunohistochemistry. DRG neurons in the compression group became swollen with vacuolar changes in cytoplasm. Decompression procedure partially ameliorated the resultant compression pathology. Ultrastructural examination showed a large number of swollen vacuoles, demyelinated nerve root fibers, absence of Schwann cells, and proliferation in the surrounding connective tissues in the compression group. Compared to the control group, the compression group showed a significant decrease in the number of the HRP-labeled cells and a significant increase in levels of PGE2 and PLA2, in the expression of VEGF protein, and in the number of apoptotic DRG neurons. These findings demonstrate that compression results in local inflammation, followed by increased apoptosis and upregulation of VEGF. We conclude that such a model provides a tool to study the pathogenesis and treatment of cervical radiculoneuropathy.

Objective: To establish a rat model of cervical syndrome with qi deficiency, blood stasis and kidney deficiency., Methods: A total of 30 three-month-old female Sprague-Dawley rats were randomly divided into normal group, cervical syndrome group and cervical syndrome with qi deficiency, blood stasis and kidney deficiency group (combined group), with 10 rats in each group. Rats in the normal group received no treatment, rats in cervical syndrome group underwent resection of cervical muscles and ligaments as unbalanced dynamic and static animal model, and rats in combined group underwent resection of both cervical muscles and ovaries, swimming and irregular diet, and injection of adrenal cortex hormone and adrenaline two and a half months after resection as combined model. The qi deficiency, blood stasis and kidney deficiency were determined by observing behaviors and physical signs of the rats, detecting the contents of plasma cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), the hemorrheology, the expression of alpha-granular membrane protein (CD62p) and the serum estradiol (E(2)) content. The aggrecan-1, type II procollagen gene (Col2a1), matrix metalloproteinases-13 (MMP-13) and tissue inhibitor of metalloproteinases-1 (TIMP-1) mRNAs in cervical intervertebral discs were detected by histopathology, immunohistochemistry and real-time polymerase chain reaction. The cataplasia of the intervertebral discs was determined by detecting the histopathology, the expressions of type II collagen and type X collegen proteins, and the expressions of aggrecan-1 (Agc1), type II procollagen gene (Col2a1), matrix metalloproteinase-13 (MMP-13) and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNAs., Results: Compared with those in the normal group and cervical syndrome group, the rats in the combined group were noted with obvious signs of deficiency of vital energy, such as depression, tiredness, ptosis, obvious weight loss and blue tail. And the ratio of cAMP/cGMP was decreased; the reducing viscosity was significantly up-regulated; the expression of CD62p was increased; the content of serum E(2) was decreased; the intervertebral disc structure was destructed; the cervical intervertebral disc was more seriously deteriorated. There exhibited a decrease in type II collagen protein expression, an increase in type X collagen protein expression, as well as decreases of Agc1, Col2a1 and TIMP-1 mRNA expressions in intervertebral disc, and the expression of MMP-13 mRNA was noted an increase., Conclusion: The rat model of cervical syndrome with qi-deficiency, blood stasis and kidney deficiency is established. Qi deficiency, blood stasis and kidney deficiency can aggravate cervical intervertebral disc degeneration.

Objective: To establish a rat model of cervical syndrome (CS) with kidney deficiency., Methods: A group of 30 three-month-old female Sprague-Dawley rats were randomly divided into normal control group, CS group and CS with kidney deficiency group (combined group), with 10 rats in each group. Rats in the normal control group received no treatment, rats in the CS group underwent only resection of cervical muscles and ligaments as unbalanced dynamic and static animal model, and rats in combined group underwent resection of both cervical muscles and ovaries as kidney deficiency model. Serum and cervical intervertebral discs were collected. Kidney deficiency was determined by observing the morphologic changes of uterus and appendages, detecting the weight of uterus and appendages and the content of serum estradiol (E(2)). The degeneration of intervertebral discs was determined by detecting the histopathology, the expressions of type II collagen and type X collagen proteins, and the expressions of aggrecan-1 (Agc1), type II procollagen gene (Col2a1), matrix metalloproteinase-13 (MMP-13) and tissue inhibitor of metalloproteinases-1 (TIMP-1) mRNAs., Results: Compared with those in the normal control group and CS group, the rats in the combined group were noted with the uterus atrophied, the caliber of oviduct thinned, the weight of uterus and appendages diminished obviously, the content of serum E(2) decreased, cervical intervertebral disc degenerated more seriously, type II collagen protein expression decreased, type X collagen protein expression increased, Agc1 and Col2a1 mRNA expressions in intervertebral disc decreased, and the MMP-13 mRNA expression increased., Conclusion: The rat model of CS with kidney deficiency is established. Kidney deficiency can aggravate cervical intervertebral disc degeneration.