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Schaftoside Ameliorates Oxygen Glucose Deprivation-Induced Inflammation Associated With the TLR4/Myd88/Drp1-related Mitochondrial Fission in BV2 Microglia Cells

Kecheng Zhou, Jiayu Wu, Jie Chen, Ye Zhou, Xiaolong Chen, Qiaoyun Wu, Yangxinzi Xu, Wenzhan Tu, Xinfa Lou, Guanhu Yang, Songhe Jiang

J Pharmacol Sci. 2019 Jan;139(1):15-22.

PMID: 30528467

Abstract:

Background:
Neuroinflammation plays a major role in the development of ischemic stroke, and regulation of the proinflammatory TLR4 signaling pathway in microglia stands to be a promising therapeutic strategy for stroke intervention. Recently, the homeostasis of mitochondrial dynamics has also been raised as a vital component in maintaining neuronal health, but its relevance in microglia hasn't been investigated. Schaftoside, a natural flavonoid compound and a promising treatment for inflammation, has demonstrated potency against LPS-induced lung inflammation in mice; however, its action on TLR4-induced neuroinflammation and mitochondrial dynamics in microglia is still unknown.
Methods:
The effects of schaftoside in regulating inflammation and mitochondrial dynamics were investigated in vitro in oxygen glucose deprivation (OGD)-stimulated BV2 microglia cells.
Results:
Schaftoside inhibited mRNA and protein expressions of proinflammatory cytokines (IL-1β, TNF-α, and IL-6) after 4 h in OGD-stimulated BV2 microglia cells, similar to the effect of TAK242, an inhibitor of TLR4. TLR4/Myd88 signaling pathway was effectively suppressed by schaftoside. In addition, both schaftoside and TAK242 treatments significantly decreased Drp1 expression, phosphorylation, translocation and mitochondrial fission in OGD-stimulated BV2 cells.
Conclusions:
Our study suggested that schaftoside was able to reduce neuroinflammation, which is mediated in part by reducing TLR4/Myd88/Drp1-related mitochondrial fission in BV2 microglia cells.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
AP51938320 Schaftoside Schaftoside 51938-32-0 Price
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