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目的:观察共轭亚油酸(CLA)对急性缺氧大鼠肝脏线粒体呼吸链酶活性及肝脏内氧化应激(OS)的影响。方法:将60只SD大鼠随机分为正常对照组,模拟海拔5000米高原环境连续缺氧暴露3d的急性缺氧组,急性缺氧CLA干预组。生化法测定肝脏组织中丙二醛(MDA)、还原型谷胱甘肽(GSH)含量及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性,Clark氧电极法观察大鼠肝脏线粒体呼吸链酶活性。结果:成功诱导大鼠急性缺氧模型。与对照组比,急性缺氧组大鼠肝脏MDA含量明显升高(P<0.05),同时肝脏线粒体呼吸链酶活性以及抗氧化酶活性(SOD,CAT)及GSH显著降低(P<0.05),与急性缺氧相比,CLA治疗组大鼠以上各项指标均有改善,并存在一定的剂量效应关系。结论:CLA通过抑制氧化应激增强大鼠肝脏线粒体呼吸链酶活性改善了急性缺氧大鼠肝脏的能量代谢障碍,对急性缺氧引起的氧化损伤有保护作用。
Objective: To observe the effect of conjugated linoleic acid (CLA) on liver mitochondrial respiratory chain enzyme activity and liver oxidative stress (OS) in acute hypoxic rats. Methods: Sixty Sprague-Dawley rats were randomly divided into normal control group, acute hypoxia group and acute hypoxia CLA intervention group. The contents of malondialdehyde (MDA), reduced glutathione (GSH) and the activity of superoxide dismutase (SOD) and catalase (CAT) in the liver tissue were measured by biochemical method. Mitochondrial respiratory chain enzyme activity. Results: Acute hypoxia model was successfully induced in rats. Compared with the control group, the content of MDA in the liver of acute hypoxia group was significantly increased (P <0.05), while the mitochondrial respiratory chain activity, antioxidant enzyme activity (SOD, CAT) and GSH were significantly decreased (P <0.05) Compared with acute hypoxia, all the above indexes in CLA treated group improved, and there was a certain dose-response relationship. CONCLUSION: CLA can enhance the hepatic mitochondrial respiratory chain enzyme activity by inhibiting oxidative stress and improve the energy metabolism of liver in acute hypoxia rats, and protect the oxidative damage induced by acute hypoxia.