一氧化氮对大鼠肝缺血-再灌注损伤中肝细胞凋亡的影响

目的探讨一氧化氮对肝缺血-再灌注损伤及肝细胞凋亡的影响。方法在一氧化氮合酶（NOS）增强剂和抑制剂条件下，观察大鼠肝缺血-再灌注后1、3、6、24h肝的血清门冬氨酸氨基转移酶（AST）和丙氨酸氨基转移酶（ALT）变化，同时进行肝细胞胞浆诱导型一氧化氮合酶（iNOS）表达及肝细胞凋亡的免疫组织化学分析。结果在再灌注6h点AST、ALT、肝细胞凋亡水平上，L-精氨酸（L-arg）组值分别为（341.88±111.24）IU/L、（311.75±139.41）IU/L和2.80±1.79，显著低于L-硝基精氨酸甲酯（L-NAME）组（2080.88±241.98）IU/L、（1153.00±110.92）IU/L和5.50±0.71（P值均＜0.05）。而L-arg组的肝细胞内iNOS表达灰度值152.07±3.46显著高于L-NAME组灰度值180.45±4.46（P＜0.05）。结论一氧化氮可减少肝缺血-再灌注损伤后肝酶的释放，抑制肝细胞的凋亡，改善肝缺血-再灌注损伤。

The influence of nitric oxide on apoptosis of hepatocytes during the rat liver ischemia-reperfusion injury

Objective　To investigate the influence of nitric oxide on apoptosis of hepatocytes during the rat liver ischemia-reperfusion injury. Methods　The changes in levels of enzymes (AST, ALT) of the liver 1, 3, 6, 24 h after ischemia-reperfusion were observed when the rats received L-arg or L-NAME respectively. Meanwhile the expression of iNOS and apoptosis of hepatocytes were detected byimmunohistochemistry method. Results　At the 6h reperfusion point, the levels of AST and ALT, the apoptosis of hepatocytes in L-arg group (341.88±111.24) IU/L, (311.75±139.41) IU/L and 2.80±1.79, respectively, significantly lower than those in the L-NAME group (2080.88±241.98 )IU/L,(1153.00±110.92)IU/L, 5.50±0.71, respectively, all P<0.05). The iNOS expression of hepatocytes in L-arg group was 152.07±3.46, significantly higher than than in the L-NAME group 180.45±4.46,( P<0.05). Conclusion　Nitric oxide could increase the release of the hepatic enzymes after liver ischemia-reperfusion injury, inhibit the apoptosis of hepatocytes and improve liver ischemia-reperfusion injury.