摘要
目的观察肝细胞线粒体钙含量变化在胆道梗阻所致肝损害中的作用及粉防己碱的保护作用。方法复制大鼠胆道梗阻模型 ,灌胃给予粉防己碱(Tet)30mg·kg-1·d -1 ,分离肝细胞线粒体 ,动态观测肝细胞线粒体钙含量 ,血清T Bil、ALT、ALP及GGT含量变化。并观察肝脏显微结构改变。结果胆道梗阻后 ,肝细胞线粒体钙含量随梗阻时间延长而逐渐升高 ,各梗阻组与对照组比较 ,P<0.05 ;血清T BiL、ALT、ALP、GGT水平随梗阻时间延长而逐渐升高(P<0.05) ;相关性分析结果表明 :胆道梗阻后 ,肝细胞线粒体钙含量与血清ALT、ALP含量变化呈明显正相关 ,r值分别为0.924和0.919 ,P<0.01。光镜下肝脏损害随梗阻时间延长而加重。各Tet治疗组与同时相的梗阻组比较 ,肝细胞线粒体钙含量减少(P<0.01) ;血清T Bil、ALT、ALP、GGT水平下降(P<0.05) ;光镜下肝脏损害程度明显减轻。结论胆道梗阻后 ,肝细胞线粒体钙超载进行性加重 ;可能是胆道梗阻导致肝损害的重要机制之一。Tet能明显减轻胆道梗阻后肝细胞线粒体钙超载程度 ,并对胆道梗阻所致肝损害有明显的保护作用。
Objective To investigate the role of the changes of hepatocytic mitochondrial calcium content and the protective effects of tetrandrine (Tet) on hepatic injury after biliary obstruction in rats. Methods After the model of complete biliary obstruction (CBO) was established in rats, Tet was administered once a day by gavage at a dose of 30 mg/kg. The contents of mitochondrial calcium and serum T-Bil, ALT, ALP and GGT were measured in each group. Hepatic morphological changes were observed under the light microscope. Results After CBO, the content of mitochondrial calcium was increased progressively (P<0.01) and those of serum T-Bil, ALT, ALP and GGT increased significantly (P<0.05). Light microscopy showed that hepatic injury was intensified progressively. The content of mitochondrial calcium was highly correlated with serum ALT and ALP. Conclusion After CBO, the calcium overload of mitochondria is intensified progressively. This may be one of the important mechanisms of hepatic injury. Tet can effectively protect the liver against the injury due to biliary obstruction.
出处
《第三军医大学学报》
CSCD
北大核心
2000年第4期369-371,共3页
Journal of Third Military Medical University
关键词
胆道梗阻
线粒体
粉防已碱
钙
鼠
肝细胞
s:biliary obstruction
liver
mitochondria
tetrandrine
calcium
rat
