缺血后处理对大鼠肝脏缺血再灌注损伤的保护作用

目的探讨缺血后处理对大鼠肝脏缺血再灌注损伤的保护作用。方法将75只SD大鼠随机分为假手术组、缺血再灌注组和缺血后处理组，建立大鼠肝脏局部缺血再灌注模型。检测大鼠血清、肝组织丙二醛（MDA）、超氧化物歧化酶（SOD）水平，并行肝组织病理学和超微结构检查及免疫组化法检测内源性一氧化氮合成酶（eNOS）的表达。结果与缺血再灌注组相比，缺血后处理组血清ALT和AST水平及肝组织MDA明显降低（P＜0．01），而SOD水平则显著升高（P〈0．01）；肝组织病理损伤减轻，在再灌注7min时IPO组肝组织eNOS蛋白表达比IR组增强。结论缺血后处理可通过抑制再灌注后氧自由基的过量生成和再灌注损伤保护激酶通路，从而减轻肝细胞损伤。

Protective effect of ischemic-postconditioning on hepatic ischemia-reperfusion injury in rats

Objective To investigate the protective effect of ischemic-postconditioning （IPO） on hepatic ischemiarepeffusion injury in rats. Methods 75 Sprague-Dawley rats were randomly divided into shamoperated （S）,ischemiareperfusion（IR） and IPO group to establish the model of acute liver ischemia-reperfusion injuries. Before persistent reperfusion,animals in IPO group were given six brief reperfusion-ischemia. The sample of blood and hepatic tissue of rats in all groups were taken for detections. Results Compared with in IR group,the concentrations of serum AST and ALT and malondialdehyde in hepatic tissues in IPO group decreased markedly （P〈0.01）,while the concentrations of superoxide dismutase increased significantly（P〈0.01 ）;the hepatic pathological damage also relieved obviously in IPO group. The expression levels of enos protein in IPO group were higher than that of IR group at the 7 rain reperfusion. Conclusion IPO can attenuate hepatic ischemia-reperfusion injury by activating the prosurvival kinases of eNOS in accordance with the RISK pathway and reducin~ the concentrations of oxwen free radical.