Berberine enhances L1 expression and axonal remyelination in rats after brachial plexus root avulsion

Background and Purpose Enhanced remyelination of the regenerated axons results in functional re‐innervation and improved functional motor recovery after brachial plexus root avulsion (BPRA). The neural cell adhesion molecule L1 (L1CAM, L1) regulates myelination and promotes regeneration after acute...

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Veröffentlicht in:Brain and behavior 2020-10, Vol.10 (10), p.e01792-n/a
Hauptverfasser: Chen, Shuangxi, He, Bing, Zhou, Guijuan, Xu, Yan, Wu, Lin, Xie, Yangzhi, Li, Yihui, Chen, Shuangqin, Huang, Jianghua, Wu, Heng, Xiao, Zijian
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Sprache:eng
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Zusammenfassung:Background and Purpose Enhanced remyelination of the regenerated axons results in functional re‐innervation and improved functional motor recovery after brachial plexus root avulsion (BPRA). The neural cell adhesion molecule L1 (L1CAM, L1) regulates myelination and promotes regeneration after acute injury in the nervous system. Berberine (BBR) can exert neuroprotective roles against the lesion. Herein, we investigated whether berberine (BBR) can affect the expression of L1 and enhance the axonal remyelination in rats following BPRA. Methods The surgical procedures were performed to build the rat brachial plexus avulsion and re‐implantation model, and then, the rats were treated with BBR. After the rehabilitation for 12 weeks, the musculocutaneous nerves were collected for quantitative real‐time PCR, Western blot analysis, and histochemical and immunofluorescence staining. Results We observed that, BBR treatment ameliorated the abnormal musculocutaneous nerve fibers morphology, up‐regulated the L1 expression, increased the myelination‐related genes, decreased the differentiated‐associated genes, and up‐regulated the phosphorylation of ERK. Conclusion These results suggest that BBR may enhance L1 expression and promote axonal remyelination after spinal root avulsion. Effect of BBR on the L1 changes in musculocutaneous nerve fibers after BPRA after BPRA in rats.
ISSN:2162-3279
2162-3279
DOI:10.1002/brb3.1792