Resveratrol promoted the M2 polarization of microglia and reduced neuroinflammation after cerebral ischemia by inhibiting miR-155

作者
Shan Ma,Lingling Fan,Junchao Li,Bei Zhang,Zhongjun Yan
出处
期刊:International Journal of Neuroscience [Taylor & Francis]
卷期号:130 (8): 817-825 被引量:58
标识
DOI:10.1080/00207454.2019.1707817
摘要

Purpose: Neuroinflammation was demonstrated to play an important role in the brain injury induced by cerebral ischemia, which was mainly mediated by microglia. MicroRNA-155 (MiR-155) was reported to promote the M1 polarization of microglia and increase neuroinflammation. Resveratrol was identified to have the ability to promote the M2 polarization of microglia and reduce inflammation. Whether resveratrol can promote the M2 polarization of microglia and further inhibit neuroinflammation after cerebral ischemia, and its correlation with miR-155 is unclear. To clarify this, we conducted this study to explore the potential of resveratrol as an effective strategy to treat cerebral ischemia induced neuroinflammation.Materials and methods:The cerebral ischemia mouse model was first constructed by middle cerebral artery occlusion (MCAO). Then resveratrol was intraperitoneally injected at 0 h, 8 h and 18 h after cerebral ischemia. Subsequently, the relative expression of miR-155 and the signature genes of M1 and M2 microglia in injured brain were measured by RT-PCR, and the concentration of pro-inflammatory and anti-inflammatory cytokines were detected by ELISA. Further, the in vitro experiments were also conducted to explore the effect of resveratrol on the inflammation mediated by LPS activated BV2 microglia.Results: Results indicated that the relative expression of miR-155 in ischemia brain and activated BV2 microglia was elevated, while resveratrol reduced the expression of miR-155. Resveratrol promoted the M2 polarization of microglia and reduced neuroinflammation in injured brain and activated BV2 microglia.Conclusions: In conclusion, this research indicated that resveratrol promoted the M2 polarization of microglia and reduced neuroinflammation after cerebral ischemia by inhibiting miR-155.

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