A Study Of Protective Effect Of Ischemic Postconditioning On Ischemia-reperfusion Injury In Rats

Objective: To investigate the protective effect of ischemic postconditioning (IPC) on ischemia-reperfusion injury and its mechanism.Methods: With a rat model of acute hepatic ischemia-reperfusion, 24 healthy male Wistar rats were randomly divided into 3 groups: sham-operated group, ischemia-reperfusion group (IR) and IPC group. IPC was achieved by several brief pre-reperfusions followed by a persistent reperfusion. The activity of plasma alanine aminotransferase (ALT), tumor necrosis factor- a (TNF- a ), interleukin-1 (IL-1 ) and the concentrations of malondialdehyde (MDA) and activity of superoxide dismutase (SOD). myeloperoxidase (MPO) in hepatic tissue were measured respectively. The apoptotic cells were detected by TdT-mediated dUTP-biotin nick end labeling (TUNEL) and the expression of Bcl-2 protein was measured by immunohistochemical techniques. Moreover, the mitochondrial ultrastructure and parameters of morphology of the above groups were observed by electron microscope.Results: Compared with IR group, the activity of plasma ALT, TNF- a , IL-1 P and the concentrations of MDA, MPO in hepatic tissue reduced markedly in IPC group(P <0.05), while the activity of SOD enhanced significantly(P<0.05). At the same time, the hepatocellular apoptotic index in IPC group reduced significantly (P<0.05), while the OD value of Bcl-2 protein enhanced markedly (P < 0.05). Moreover, the injury of mitochondrial ultrastructure in IPC group also relieved obviously.Conclusion: Proinflammatory. cytokines such as TNF- a , IL-1 3 mediate neutrophil-induced hepatic ischemia-reperfusion injury. IPC can reduce the synthesis of oxygen free radicals and the secretion of proinflammatory cytokines after reperfusion, then attenuate the neutrophilic infitration in hepatic tissue and relieve hepatic injury. Moreover, IPC can protect the mitochondrial ultrastructure and increase the expression of Bcl-2 protein that lies across the mitochondrial membrane. Consequently, IPC can reduce the hepatocellular apoptosis after reperfusion and has a protective effect on hepatic ischemia-reperfusion injury.