miR-652 protects rats from cerebral ischemia/reperfusion oxidative stress injury by directly targeting NOX2

Biomedicine & Pharmacotherapy

Zhong-Bao Yang¹  Ai-Ping Wang²  Mei-Ling Zuo³  Gui-Lin Song³ 

[1] Institute of Emergency and Critical Care Medicine of Changsha, Changsha, China;Institute of Clinical Research, Affiliated Nanhua Hospital, University of South China, Hengyang, 421001, Hunan, China;Office of Good Clinical Practice, The Affiliated Changsha Hospital of Hunan Normal University, Changsha, 410006, Hunan, China;

关键词: Cerebral ischemia/reperfusion injury;    Oxidative stress;    NOX2;    miR-652;   

DOI  :  

来源: DOAJ

【 摘 要 】

Ischemic stroke is a devastating central nervous disease associated with oxidative stress and NOX2 is the main source of ROS responsible for brain tissue. miRNAs are a class of negative regulator of genes in mammals and involves the pathogenesis of ischemic stroke. This study aims to observe the role of target miRNA(miR-652) of NOX2 in ischemic stroke. A rat cerebral ischemia/reperfusion (CI/R) injury model and an SH-SY5Y cell hypoxia/reoxygenation(H/R) model were used to simulate ischemic stroke, and corresponding gene expression, biochemical indicators and pathophysiological indicators were measured to observe the role of miR-652. NOX2 significantly increased in brain tissues subjected to I/R or in SH-SY5Y cells subjected to H/R, while the expression level of miR-652(potential target of NOX2) significantly decreased in both brain tissues and plasma. Overexpression of miR-652 significantly suppressed NOX2 expression and ROS generation in H/R treated SH-SY5Y cells and reduced the relative luciferase activity of cells transfected with plasmid NOX2-WT (reporter gene plasmid). MiR-652 agomir significantly decreased the expression of NOX2 and ROS generation in brain tissues of CIR rats, as well as tissue injury. These data indicated that miR-652 protected rats from cerebral ischemia reperfusion injury by directly targeting NOX2, is a novel target for ischemic stroke therapy.

【 授权许可】

Unknown