Basic Research
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 1, 2004; 10(13): 1934-1938
Published online Jul 1, 2004. doi: 10.3748/wjg.v10.i13.1934
Role of mitochondria in cell apoptosis during hepatic ischemia-reperfusion injury and protective effect of ischemic postconditioning
Kai Sun, Zhi-Su Liu, Quan Sun
Kai Sun, Zhi-Su Liu, Quan Sun, Department of General Surgery, Zhongnan Hospital, Wuhan University, Wuhan 430071, Hubei Province, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Professor Zhi-Su Liu, Department of General Surgery, Zhongnan Hospital, Wuhan University, Wuhan 430071, Hubei Province, China. hyfr@mail.wh.cei.gov.cn
Telephone: +86-27-87331752 Fax: +86-27-87330795
Received: June 28, 2003
Revised: October 5, 2003
Accepted: October 12, 2003
Published online: July 1, 2004
Abstract

AIM: To investigate the role of mitochondria in cell apoptosis during hepatic ischemia-reperfusion injury and protective effect of ischemic postconditioning (IPC).

METHODS: A rat model of acute hepatic ischemia-reperfusion was established, 24 healthy male Wistar rats were randomly divided into sham-operated group, ischemia-reperfusion group (IR) and IPC group. IPC was achieved by several brief pre-reperfusions followed by a persistent reperfusion. Concentration of malondialdehyde (MDA) and activity of several antioxidant enzymes in hepatic tissue were measured respectively. Apoptotic cells were detected by TdT-mediated dUTP-biotin nick end labeling (TUNEL) and expression of Bcl-2 protein was measured by immunohistochemical techniques. Moreover, mitochondrial ultrastructure and parameters of morphology of the above groups were observed by electron microscope.

RESULTS: Compared with IR group, the concentration of MDA and the hepatocellular apoptotic index in IPC group was significantly reduced (P < 0.05), while the activity of antioxidant enzymes and OD value of Bcl-2 protein were markedly enhanced (P < 0.05). Moreover, the injury of mitochondrial ultrastructure in IPC group was also obviously relieved.

CONCLUSION: IPC can depress the synthesis of oxygen free radicals to protect the mitochondrial ultrastructure and increase the expression of Bcl-2 protein that lies across the mitochondrial membrane. Consequently, IPC can reduce hepatocellular apoptosis after reperfusion and has a protective effect on hepatic ischemia-reperfusion injury.

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