| Literature DB >> 32791262 |
Weixiang Chen1, Chao Guo1, Suna Huang1, Zhengcai Jia1, Jie Wang1, Jun Zhong1, Hongfei Ge1, Jichao Yuan2, Tunan Chen1, Xin Liu1, Rong Hu3, Yi Yin4, Hua Feng5.
Abstract
Microglial phenotype plays an important role in secondary injury after intracerebral haemorrhage (ICH), with M1 microglia promoting inflammatory injury and M2 microglia inhibiting neuroinflammation and promoting haematoma absorption. However, there is no effective intervention for regulating the phenotypic transformation of microglia after ICH. This study aimed to elucidate the protective effect of MitoQ, a selective mitochondrial ROS antioxidant, against microglial M1 state polarization and secondary brain injury. The in vivo data showed that MitoQ attenuated neurological deficits and decreased inflammation, oedema and haematoma volume after ICH. In addition, MitoQ decreased the expression of M1 markers and increased the expression of M2 markers both in vivo and in vitro after ICH. Mechanistically, MitoQ blocked overproduction of mitochondrial ROS and activation of the NLRP3 inflammasome in FeCl2-treated microglia. Moreover, NLRP3 siRNA shifted FeCl2-treated microglia from the M1 to the M2 cells, revealing that MitoQ-induce polarization states may be mediated by the mitochondrial ROS/NLRP-3 pathway. In summary, MitoQ alleviates secondary brain injury and accelerates haematoma resolution by shifting microglia towards the M2 phenotype after ICH.Entities:
Keywords: Intracerebral haemorrhage; Microglia polarization; Mitochondrial reactive oxygen species; Mitoquinone (MitoQ); NLRP3; Secondary brain injury
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Year: 2020 PMID： 32791262 DOI： 10.1016/j.phrs.2020.105122
Source DB: PubMed Journal: Pharmacol Res ISSN： 1043-6618 Impact factor: 7.658