缺血
细胞凋亡
清道夫受体
再灌注损伤
氧化应激
药理学
内生
自由基清除剂
受体
医学
体内
生物
癌症研究
化学
内科学
生物化学
生物技术
胆固醇
脂蛋白
作者
Chun Chen,Xiaolong Chang,Shifei Zhang,Qi Zhao,Chunyan Lei
出处
期刊:Bioengineered
[Informa]
日期:2022-04-01
卷期号:13 (4): 10258-10273
被引量:6
标识
DOI:10.1080/21655979.2022.2061304
摘要
Emerging studies show that circRNA catenin beta 1 (circCTNNB1) plays a critical role in cancer. However, the expression and function of circCTNNB1 in cerebral ischemia/reperfusion injury (IRI) have not been reported. The present study discovered that circCTNNB1 and scavenger receptor class B type 1 (SRB1) expression levels were significantly down-regulated in mouse astrocytes (mAS) treated with oxygen glucose deprivation and reperfusion (OGD/R), and similar results were observed in a mouse middle cerebral artery occlusion model. Overexpression of circCTNNB1 alleviated cell apoptosis, oxidative stress and the inflammatory response induced by OGD/R in vitro. Up-regulation of circCTNNB1 increased SRB1 expression levels to protect mAS cells from OGD/R-induced damage. CircCTNNB1 and SRB1 interacted with miR-96-5p, and the overexpression of miR-96-5p efficiently reversed the function of circCTNNB1 in OGD/R-treated mAS cells. CircCTNNB1 protected against cerebral ischemia-reperfusion injury by up-regulating SRB1 in vivo. In conclusion, our findings suggest that circCTNNB1 acts as a competitive endogenous RNA for miR-96-5p to alleviate cerebral IRI, which provides novel evidence that circCTNNB1 and SRB1 may be biomarkers and therapeutic targets for cerebral IRI.
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