miR-652 protects rats from cerebral ischemia/reperfusion oxidative stress injury by directly targeting NOX2 - 11/02/20
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Abstract |
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.
Le texte complet de cet article est disponible en PDF.Abbreviations : CI/R, H/R, NOX2, TUNEL, MCAO, SOD, GSH-Px, ROS
Keywords : Cerebral ischemia/reperfusion injury, Oxidative stress, NOX2, miR-652
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Vol 124
Article 109860- avril 2020 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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