摘要：

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 (0.05), while the activity of antioxidant enzymes and OD value of Bcl-2 protein were markedly enhanced (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.Hepatic ischemia-reperfusion injury (IRI) is a common pathological process of traumatic surgical diseases in the liver, such as severe liver trauma, extensive hepatic lobus excision, liver transplantation, shock and infection. When hepatic IRI happens, a series of metabolic and structural and functional disorder of hepatic tissue cells would occur, which directly influence the prognosis of patients. At present, the study about the mechanism and intervention method of hepatic IRI has been carried out extensively. It has been confirmed that apoptosis as a way of cell death is significant for maintaining normal cell development and stabilization, and is closely related to the initiation and development of many clinical diseases, and it also participates in IRI of tissues and organs. Mitochondria as one of the organelle of cells play an important role in providing energy, adjusting osmotic pressure, calcium balance, and pH value, and cell signaling. Mitochondria perform their function by production of ATP and reactive oxygen species (ROS) which are also known as signals regulating gene expression and triggering cell death. At present, mitochondria/ cytochrome C apoptotic pathway has attracted close attention of scholars. Many stimulators such as ROS, Caand cytokines could activate cysteine aspartate-specific proteases (Caspase) by inducing cytochrome C release. But the study on the changes of the structure and function of mitochondria in hepatic IRI and the adjusting function of mitochondria in hepatocellular apoptosis was rarely reported at home and abroad. We established a hepatic IRI model in liver of rats, and observed the influence of ischemic postconditioning (IPC) on cell apoptosis in hepatic IRI and the adjustment function of mitochondria. This experiment lays a theoretical foundation for adopting a more reasonable method to restore the blood flow after hepatic ischemia.Twenty-four healthy male Wistar rats, weighing 200-250 g, were supplied by the Experimental Animal Center of Wuhan University. Malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-PX) assay kits were purchased from Nanjing Jiancheng Bioengineering Co.Ltd, China. Mouse anti-rat Bcl-2 monoclonal antibody and SP assay kit were provided by Beijing Zhongshan Biotechnology Co.Ltd, China. Terminal deoxynucleotidyl transferase (TdT) mediated dUTP nick end labeling (TUNEL) in situ cell death detection kit was the product of Boehringer Mannhein Co.Ltd, USA.The animals were fed standard laboratory

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