Inhibition of P2X4R attenuates white matter injury in mice after intracerebral hemorrhage by regulating microglial phenotypes.
Xiongjie FuGuoyang ZhouXinyan WuChaoran XuHang ZhouJianfeng ZhuangYucong PengYang CaoHanhai ZengYin LiJianru LiLiansheng GaoChen GaoLin WangFeng YanPublished in: Journal of neuroinflammation (2021)
Our results demonstrated that P2X4R contributes to WMI by polarizing microglia into a pro-inflammatory phenotype after ICH. Furthermore, the inhibition of P2X4R promoted pro-inflammatory microglia polarization into an anti-inflammatory phenotype, enhanced brain-derived neurotrophic factor (BDNF) production, and through the BDNF/TrkB pathway, attenuated WMI and improved neurological function. Therefore, the regulation of P2X4R activation may be beneficial for the reducing of ICH-induced brain injury.
Keyphrases
- brain injury
- inflammatory response
- subarachnoid hemorrhage
- white matter
- neuropathic pain
- cerebral ischemia
- anti inflammatory
- stress induced
- lipopolysaccharide induced
- high glucose
- lps induced
- diabetic rats
- multiple sclerosis
- spinal cord
- spinal cord injury
- type diabetes
- oxidative stress
- endothelial cells
- high fat diet induced
- wild type