摘要
目的探讨继发性胆汁性肝硬化时肝线粒体呼吸功能及呼吸酶的损伤及其机制。方法双重结扎犬胆总管5周复制继发性胆汁性肝硬化模型，用差速离心法分离肝线粒体，观察肝线粒体呼吸功能，线粒体院琥珀酸脱氢酶（SDH）、细胞色素C氧化酶（CCO）活力及线粒体Ca2+、丙二醛（MDA）、超氧化物歧化酶（SOD）含量变化。结果继发性胆汁性肝硬化时肝线粒体呼吸功能、呼吸酶SDH及CCO活力均显著降低，线粒体Ca2+及MDA含量明显升高，SOD含量则显著下降。结论继发性胆汁性肝硬化时肝线粒体呼吸功能及呼吸酶系受到明显损伤，钙超载及脂质过氧化反应是造成线粒体损伤的重要原因。
Objective To explore the damage of liver mitochondrial respiratory function、respiratory enzymes and its mechanisms in secondary binary cirrhosis. Methods The model of secondary binary cirrhosis in dogs was made by bile duct ligation for 5weeks. Mitochondrium were obtained by differential centrifugation, mitochondrial respiratory function,the activity of SDH、CCO andthe contents of Ca2+、MDA、SOD were measured. Results The liver mitochondrial respiratory function and the activites of SDH、CCO were decreased significantly,and the contents of Ca2+ and MDA were obviously increased with significant decreased in SODcontent. Conclusions The liver mitochondrial respiratory function and the activites of respiratory enzymes are damaged significantly in secondary binary cirrhosis,calcium overload and lipid peroxidation may be the main mechanisms of mitochondrial dysfunctlon.
出处
《肝胆外科杂志》
1999年第1期67-69,共3页
Journal of Hepatobiliary Surgery
关键词
肝硬化
胆汁法
肝线粒体
钙
呼吸酶损伤
篖iver cirrhosis,biliary, Mitochondria,liver，Calcium，Lipid peroxidation
