Rg1 exerts protective effect in CPZ-induced demyelination mouse model via inhibiting CXCL10-mediated glial response

• DOI: 10.1038/s41401-021-00696-3
• Publication Date: 2021-06-08T08:03:10Z
• Authors: Yi-xiao Dong; Shi-feng Chu; Sha-sha Wang; Ya-juan Tian; Wen-bin He; Yu-sheng Du; Zhen-zhen Wang; Xu Yan; Zhao Zhang; Nai-hong Chen
• Keywords: Remyelination

Myelin damage and abnormal remyelination processes lead to central nervous system dysfunction. Glial activation-induced microenvironment changes are characteristic features of the diseases with myelin abnormalities. We previously showed that ginsenoside Rg1, a main component ginseng, ameliorated MPTP-mediated in mice, but underlying mechanisms unclear. In this study we investigated effects Rg1 cuprizone (CPZ)-induced demyelination mouse model. Mice were treated CPZ solution (300 mg· kg−1· d−1, ig) for 5 weeks; from week 2, mice received (5, 10, 20 4 weeks. administration dose-dependently alleviated bradykinesia improved CPZ-disrupted motor coordination ability CPZ-treated mice. Furthermore, significantly decreased axonal injury pathological assays. further revealed neuroprotective associated inhibiting CXCL10-mediated modulation glial response, which was mediated by NF-κB nuclear translocation CXCL10 promoter activation. microglial cell line BV-2, demonstrated on pro-inflammatory migratory phenotypes microglia related CXCL10, while Rg1-induced phagocytosis not directly CXCL10. CPZ-induced model, injection AAV-CXCL10 shRNA into lateral ventricles 3 weeks prior treatment occluded beneficial behavioral conclusion, mediates protective role This provides new insight potential disease-modifying therapies