Sevoflurane Postconditioning Protects Isolated Rat Hearts Against Ischemia-reperfusion Injury: the Role of Radical Oxygen Species, Extracellular Signal-related Kinases 1/2 and Mitochondrial Permeability Transition Pore

Overview

Journal Mol Biol Rep

Specialty Molecular Biology

Date 2009 Aug 21

PMID 19693689

Citations 22

Authors

Yun-Tai Yao

Li-Huan Li

Lei Chen

Wei-Peng Wang

Li-Bing Li

Chang-Qing Gao

Affiliations

Soon will be listed here.

Abstract

The roles of reactive oxygen species (ROS), extracellular signal-regulated kinase 1/2 (ERK 1/2) and mitochondrial permeability transition pore (mPTP) in sevoflurane postconditioning induced cardioprotection against ischemia-reperfusion injury in Langendorff rat hearts were investigated. When compared with the unprotected hearts subjected to 30 min of ischemia followed by 1 h of reperfusion, exposure of 3% sevoflurane during the first 15 min of reperfusion significantly improved functional recovery, decreased infarct size, reduced lactate dehydrogenase and creatine kinase-MB release, and reduced myocardial malondialdehyde production. However, these protective effects were abolished in the presence of either ROS scavenger N-acetylcysteine or ERK 1/2 inhibitor PD98059, and accompanied by prevention of ERK 1/2 phosphorylation and elimination of inhibitory effect on mPTP opening. These findings suggested that sevoflurane postconditioning protected isolated rat hearts against ischemia-reperfusion injury via the recruitment of the ROS-ERK 1/2-mPTP signaling cascade.

Citing Articles

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