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Objective: To investigate ischemia after treatment on hepatic ischemia reperfusion Bcl -2 and Bax protein expression and its mechanism . Methods: 45 healthy male SD rats were randomly divided into three groups: sham operation group (S group) , ischemia-reperfusion group (I / R group) , the ischemic postconditioning the group (IPo group ) , n = 15 only . Establishment of a rat partial liver ischemia-reperfusion model , in group IPo was rat liver in recovery comprehensive blood reperfusion given before reperfusion 10s, ischemic 10s , repeated 6 times after ischemia treatment , the three groups of animals in the reperfusion , 4,6 h detection of ALT and AST, blood samples were cut liver tissue detected MDA , the SOD preparation of pathological ultrastructure of mitochondria in electron microscopy ; liver tissue were detected by immunohistochemical method of Bcl-2Bax protein expression . Results: Compared with IR group each time point the group IPo serum ALT, AST levels after reperfusion was significantly lower ( P <0.01 ) . 2. Compared with IR group , reperfusion at each time point the group IPo liver tissue MDA content significantly decreased ( P <0.01 ) , SOD activity was significantly higher ( P <0.05 ) . 2,4,6 h liver pathology morphological changes of the light in the IR group 3.IPo group after reperfusion . Group 4.IPo Bcl-2 protein expression was significantly higher than in IR group ( P <0.01 ) , and Bax protein expression was significantly lower than the IR group ( P <0.01 ) . Conclusion : Bcl-2, Bax protein expression changes involved in hepatocyte apoptosis and ischemia-reperfusion injury ; ischemia after treatment can significantly reduce hepatocyte apoptosis , inhibition of ischemia-reperfusion injury . Reduction of hepatic apoptosis and upregulation of Bcl-2 gene protein , Bax downregulation .
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