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Propofol protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via Akt activation and Bcl-2 up-regulation

TitlePropofol protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via Akt activation and Bcl-2 up-regulation
Publication TypeJournal Article
Year of Publication2009
AuthorsWang, BH, Shravah, J, Luo, HL, Raedschelders, K, Chen, DDY, Ansley, DM
JournalBiochemical and Biophysical Research Communications
Volume389
Pagination105-111
Date PublishedNov
Type of ArticleArticle
ISBN Number0006-291X
Keywords15-F-2T-ISOPROSTANE FORMATION, Akt, antioxidant capacity, apoptosis, Bcl-2, CARDIOMYOCYTES, ENDOTHELIAL-CELLS, H9c2 cells, INJURY, KINASE-C, OXIDATIVE STRESS, Propofol, RAT-HEART, REDUCES APOPTOSIS, REPERFUSION, SENSITIVITY, SURVIVAL
Abstract

Propofol is a widely used intravenous anesthetic agent with antioxidant properties secondary to its phenol based chemical structure. Treatment with propofol has been found to attenuate oxidative stress and prevent ischemia/reperfusion injury in rat heart. Here, we report that propofol protects cardiac H9c2 cells from hydrogen peroxide (H2O2)-induced injury by triggering the activation of Akt and a parallel up-regulation of Bcl-2. We show that pretreatment with propofol significantly protects against H2O2-induced injury. We further demonstrate that propofol activates the PI3K-Akt signaling pathway. The protective effect of propofol on H2O2-induced injury is reversed by PI3K inhibitor wortmannin, which effectively suppresses propofol-induced activation of Akt, up-regulation of Bcl-2, and protection from apoptosis. Collectively, our results reveal a new mechanism by which propofol inhibits H2O2-induced injury in cardiac H9c2 cells, supporting a potential application of propofol as a preemptive cardioprotectant in clinical settings such as coronary bypass surgery. (C) 2009 Elsevier Inc. All rights reserved.

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