摘要：

AIM:To investigate the role of mitochondria in cell apoptosisduring hepatic ischemia-reperfusion injury and protectiveeffect of ischemic postconditioning (IPC).METHODS:A rat model of acute hepatic ischemia-reperfusionwas established,24 healthy male Wistar rats were randomlydivided into sham-operated group,ischemia-reperfusiongroup (IR) and TPC group.IPC was achieved by severalbrief pre-reperfusions followed by a persistent reperfusion.Concentration of malondialdehyde (MDA) and activity ofseveral antioxidant enzymes in hepatic tissue were measuredrespectively.Apoptotic cells were detected by TdT-mediateddUTP-biotin nick end labeling (TUNEL) and expression ofBcl-2 protein was measured by immunohistochemicaltechniques.Moreover,mitochondrial ultrastructure andparameters of morphology of the above groups were obsewedby electron microscope.RESULTS:Compared with IR group,the concentration ofMDA and the hepatocellular apoptotic index in IPC groupwas significantly reduced (P<0.05),while the activity ofantioxidant enzymes and OD value of Bcl-2 protein weremarkedly enhanced (P<0.05).Moreover,the injury ofmitochondrial ultrastructure in IPC group was also obviouslyrelieved.CONCLUSION:IPC can depress the synthesis of oxygenfree radicals to protect the mitochondrial ultrastructure andincrease the expression of Bd-2 protein that lies across themitochondrial membrane.Consequently,IPC can reducehepatocellular apoptosis after reperfusion and has aprotective effect on hepatic ischemia-reperfusion injury.

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