胆盐诱发肝细胞凋亡及蛋白激酶C信号通道的作用  

Bile salt induces apoptosis of hepatocytes and the role of protein kinase C signal pathway in obstructive jaundice.

作　　者：王剑明[1] 邹声泉[1] 

机构地区：[1]同济医科大学附属同济医院外科,武汉市430030

出　　处：《中华肝胆外科杂志》2000年第4期291-293,共3页Chinese Journal of Hepatobiliary Surgery

摘　　要：目的　从细胞凋亡的角度探讨阻塞性黄疸肝损害的调控机理。方法　采用胶原酶原位肝灌注法获取大鼠肝细胞 ,行原代培养 ,使用不同浓度甘氨鹅脱氧胆酸钠 (GCDC)及蛋白激酶C激动剂PMA、拮抗剂白屈菜赤碱 (chelerythrine)作用肝细胞后 ,用流式细胞术 (FCM)分析肝细胞的凋亡比率 ,用生物素 dUTP标记的TUNEL技术进行凋亡的原位检测。结果　随GCDC浓度的增加 ,肝细胞的凋亡比率明显增加 ,15 0 μMGCDC作用后肝细胞的凋亡率达到 (38 2 3± 1 5 8) % ;随PMA浓度的增加 ,肝细胞的凋亡明显增加 ,随白屈菜赤碱的增加 ,肝细胞的凋亡明显减少。结论　胆盐致肝细胞的凋亡 ,这可能是阻塞性黄疸肝损害的机理 ,蛋白激酶C信号通道起重要的调控作用。Objective To study the regulating mechanism of hepatic injury in obstructive jaundice by comparing apoptotic rate. Methods Rat hepatocytes were isolated by in situ collagenase perfusion and primary culture. After hepatocytes were added with different concentration of glycochenodeoxycholate (GCDC)/PKC agonist PMA and inhibitor chelerythrine, cells were evaluated by FCM and dUTP labeling TUNEL. Results The apoptotic rate was related to concentraton of GCDC: (38.23±1.58)% of hepatocytes were apoptotic by 150 μM GCDC. PMA increased GCDC induced apoptosis while chelerythrine decreased it in a concentration dependent manner. Conclusions The mechanism of hepatic injury in obstructive jaundice is related to bile salt caused hepatocyte apoptosis. PKC signal pathway might be important in the regulation of apoptosis in obstructive jaundice.

关 键 词：胆盐 肝细胞凋亡 蛋白激酶C 阻塞性黄疸 

分 类 号：R363[医药卫生—病理学]