| Literature DB >> 28274860 |
Xinchun Ye1, Tong Shen1, Jinxia Hu1, Liang Zhang1, Yunshan Zhang1, Lei Bao1, Chengcheng Cui1, Guoliang Jin1, Kun Zan1, Zuohui Zhang1, Xinxin Yang1, Hongjuan Shi1, Jie Zu1, Ming Yu2, Chengjie Song3, Yulan Wang4, Suhua Qi5, Guiyun Cui6.
Abstract
Previous research has shown that Purinergic 2X7 receptor (P2X7R) and NLRP3 inflammasome contribute to the inflammatory activation. In this study, we investigated whether P2X7R/NLRP3 pathway is involved in the caspase-3 dependent neuronal apoptosis after ischemic stroke by using a focal cortex ischemic stroke model. The expressions of P2X7R, NLRP3 inflammsome components, and cleaved caspase-3 were significantly enhanced in the ischemic brain tissue after stroke. However, the expression of cleaved caspase-3 was significantly attenuated after treatment of stroke with P2X7R antagonist (BBG) or NLRP3 inhibitor (MCC950). The treatment also significantly reduced the infarction volume, neuronal apoptosis, and neurological impairment. In addition, in vitro data also support the hypothesis that P2X7R/NLRP3 pathway plays a vital role in caspase-3 dependent neuronal apoptosis after ischemic stroke. Further investigation of effective regulation of P2X7R and NLRP3 in stroke is warranted.Entities:
Keywords: Caspase-3; Ischemic stroke; NLRP3 inflammasome; Neuronal apoptosis; P2X7 receptor
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Year: 2017 PMID： 28274860 DOI： 10.1016/j.expneurol.2017.03.002
Source DB: PubMed Journal: Exp Neurol ISSN： 0014-4886 Impact factor: 5.330