Dynamic Balance of Microglia and Astrocytes Involved in the Remyelinating Effect of Ginkgolide B

• Published in: Frontiers in cellular neuroscience Vol. 13; p. 572
• Main Authors: Yin, Jun-Jun, He, Yan, An, Jun, Miao, Qiang, Sui, Ruo-Xuan, Wang, Qing, Yu, Jie-Zhong, Xiao, Bao-Guo, Ma, Cun-Gen
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Research Foundation 08.01.2020; Frontiers Media S.A
• Subjects: Animal cognition; Anxiety; Astrocytes; Cellular Neuroscience; Central nervous system; Cognitive ability; Cuprizone; cuprizone-induced demyelination; Demyelination; Disease; Experiments; Ginkgolide B; Ginkgolides; Glial stem cells; Hypoxia; IL-1β; Ischemia; Laboratory animals; Microglia; Multiple sclerosis; Myelin; Myelination; Neurological diseases; Neurons; Neuroprotection; Neurotrophic factors; NF-κB protein; Nitric-oxide synthase; Oxidative stress; Proteins; remyelination; TLR4 protein; Toll-like receptors; Tumor necrosis factor-α; United States > US; China; astrocytes; microglia; Ginkgolide B; cuprizone-induced demyelination; remyelination
• ISSN: 1662-5102; 1662-5102
• DOI: 10.3389/fncel.2019.00572

Multiple sclerosis (MS) is an inflammatory demyelinating disorder in the central nervous system (CNS), in which remyelination failure results in persistent neurologic impairment. Ginkgolide B (GB), a major terpene lactone and active component of Ginkgo biloba, has neuroprotective effects in several models of neurological diseases. Here, our results show, by using an cuprizone (CPZ)-induced demyelinating model, administration of GB improved behavior abnormalities, promoted myelin generation, and significantly regulated the dynamic balance of microglia and astrocytes by inhibiting the expression of TLR4, NF-κB and iNOS as well as IL-1β and TNF-α, and up-regulating the expression of Arg-1 and neurotrophic factors. GB treatment also induced the generation of oligodendrocyte precursor cells (OPCs). cell experiments yielded the results similar to those of the model. The dynamic balance by decreasing microglia-mediated neuroinflammation and promoting astrocyte-derived neurotrophic factors should contribute to endogenous remyelination. Despite GB treatment may represent a novel strategy for promoting myelin recovery, the precise mechanism of GB targeting microglia and astrocytes remains to be further explored.