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Chinese Archives of General Surgery(Electronic Edition) ›› 2009, Vol. 03 ›› Issue (02): 24-26. doi: 10.3877/cma.j.issn.1674-0793.2009.02.008

• Original Articles • Previous Articles     Next Articles

Effect of ischemic postconditioning on cells apoptosis and Bcl-2 and Bax expression in rat liver after ischemia-reperfusion injury

Qiang WANG1, Zhi-peng LIANG1,(), Guang-jie NIE1, Fei-wen DENG1   

  1. 1.Department of Hepatobiliary Surgery, the Affiliated Zhanjiang Central Hospital, Guangdong Medical College, Zhanjiang 524037, China
  • Received:2008-10-06 Online:2009-04-01 Published:2024-11-30
  • Contact: Zhi-peng LIANG

Abstract:

Objective

To investigate the effect of ischemic postconditioning (IPC)on apoptosis and the expression of Bcl-2 and Bax in hepatic tissue after early ischemia-reperfusion injury and its mechanism.

Methods

A rat model of acute hepatic ischemia-reperfusion was established. Fifty-four male Sprague-Dawley rats were randomly allocated into sham-operated(SO)group,ischemia-reperfusion(IR)group and ischemic postconditioning (IPC)group.IPC was achieved by several brief episodes of reperfusion before the persistent reperfusion procedure.The activity of plasma enzyme and expressions of Bcl-2 and Bax in hepatic tissue were measured respectively at 1,3,6 h after reperfusion.The apoptosis in hepatic tissue was assessed by TUNEL method.

Results

Compared with SO group, the activity of plasma enzyme and expression of Bax increased and the expression of Bcl-2 reduced in IR group.There were obvious apoptosis in IR group.While compared with IR group,the activity of plasma enzyme and expression of Bax were reduced and the expression of Bcl-2 was increased in IPC group. The apoptotic index in IPC group was lower than in IR group.The difference were statistically significant.

Conclusions

IPC can relieve the hepatic ischemia-reperfusion injury in rat liver.IPC may inhibit apoptosis in hepatic tissue by up-regulating Bcl-2 and down-regulating Bax, thus produce a protective effect on hepatic ischemia-reperfusion injury.

Key words: Hepatocytes, Reperfusioninjury, Apoptosis, Bcl-2, Bax

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