论文部分内容阅读
目的 :探讨内源性一氧化氮 (NO)对大鼠肝缺血再灌注损伤的作用及其与脂质过氧化的关系 ;方法 :以缺血再灌注制成大鼠模型 ,以工具药L -精氨酸 (L -arg)为外源性NO的激动剂 ,观察内源性NO对肝脏损伤程度和脂质过氧化终产物丙二醛 (MDA)含量的影响 ;结果 :缺血再灌注可造成肝组织损伤 ,MDA含量增加 ,内源性NO水平降低 ,与对照组比较 (P <0 .0 1 )。以L -arg激动内源性NO ,可明显减轻肝组织损伤程度 ,同时MDA含量降低 ,NO水平升高 ,与IR组比较 (P <0 .0 5) ;结论 :内源性NO具有肝脏保护作用 ,其保护机制可能与抗氧自由基有关。
AIM: To investigate the effect of endogenous nitric oxide (NO) on hepatic ischemia-reperfusion injury in rats and its relationship with lipid peroxidation.METHODS: A rat model of ischemia-reperfusion was established. The drug L - L-arginine (L-arginine) is an exogenous NO agonist. The effects of endogenous NO on liver injury and the content of malondialdehyde (MDA) in lipid peroxidation products were observed. Results: Can cause liver tissue damage, MDA content increased, endogenous NO levels decreased, compared with the control group (P <0.01). L-arg activation endogenous NO, can significantly reduce the degree of liver damage, while MDA content decreased, the level of NO increased, compared with the IR group (P <0.05); Conclusion: endogenous NO with liver protection Role, its protective mechanism may be related to antioxidant free radicals.