| AIM: To investigate the role of mitochondria during acute hepatic ischemia-reperfusion injury and protective effect of ischemic postconditioning (IP) and the propriate time of IP.METHODS: A rat model of acute hepatic ischemia-reperfusion was established, 24 healthy male SD rats were randomly divided into sham-operated group, ischemia-reperfusion group (IR), 10- minute IP group and 20-minute IP group. IP was achieved by several brief pre-reperfusions followed by a persistent reperfusion. Expression of ALT, AST and LDH were measured by biochemical techniques. Concentration of antioxygen free radicals (AFR), GSH and activity of ATP enzymes in hepatic tissue were measured respectively. Apoptotic cells were detected by TdT-mediated dUTP-biotin nick end labeling (TUNEL) and change of mitochondrial membrane potential(MMP) was measured by DiOC6. Moreover, mitochondrial ultrastructure and parameters of morphology of the above groups were observed by optical and electron microscope.RESULTS: Compared with IR group, the activity of ATPase and the hepatocellular apoptotic index in 10-minute IP group was significantly reduced (P<0.05), while the concentration of ALT, AST, LDH, GSH, AFR and mitochondrial membrane potential were markedly enhanced (P<0.05). Moreover, the injury of mitochondrial ultrastructure in 10-minute IP group was also obviously relieved. But there is no obviously changes in 20-minute IP group.CONCLUSIONS: 10-minute IP can protect liver mitochondria by four ways as followed:(1)up-regulate the mitochondrial membrane potential to decrease mitochondrial membrane permeability; (2) enhance AFR and GSH to depress the synthesis of oxygen free radicals to protect the mitochondrial ultrastructure ;(3)decrease the activity of ATPase in... |
