阻塞性黄疸大鼠肝组织细胞凋亡及相关基因bcl-2、bax的表达  

Apoptosis of hepatocytes in rat of obstructive jaundice and expression of apoptotic related genes bcl-2 and bax

作　　者：王剑明[1] 孙宏武 邹倩[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430030 [2]湖北大冶特钢集团公司医院

出　　处：《中华实验外科杂志》2000年第1期32-33,共2页Chinese Journal of Experimental Surgery

摘　　要：目的　探讨阻塞性黄疸肝损害的调控机制。方法　用末端脱氧核苷酸转移酶介导生物素标记(TUNEL)技术和免疫组织化学方法检测 4 0只阻塞性黄疸大鼠肝脏组织细胞凋亡状态及凋亡相关基因bcl 2和bax蛋白的表达。结果　胆总管结扎后 ,随结扎时间的延长细胞凋亡增加 ,结扎 14d后细胞凋亡达高峰 ,凋亡指数 (AI)达 5 8.2 3± 1.5 8,各组AI差异有显著性 (P <0 .0 5 )。在阻塞性黄疸过程中 ,bcl 2蛋白表达越强 ,bax蛋白表达越弱 ,AI亦越少。结论　bcl 2和bax蛋白均参与了阻塞性黄疸肝组织中细胞凋亡的调节。Objective\ To explore the regulating mechanism of hepatic injury in obstructive jaundice (OJ). Methods\ The apoptotic status and the expression of apoptotic related gene bcl 2 and bax protein in liver of OJ were detected by using terminal deoxynucleotidyl mediated nick end labeling (TUNEL) and immunohistochemistry method. Results\ The apoptotic rate of liver was related to the duration of OJ. Apoptosis reached the highest after 14 day bile duct ligation, apoptotic index (AI) was 58.23±1.58 ( P <0.05). The stronger bcl 2 expression was, the weaker bax expression and the less number of apoptotic cells in OJ. Conclusion\ Both bcl 2 and bax might take part in the regulation and the development and progression of hepatic injury in OJ.

关 键 词：阻塞性黄疸 肝损害 细胞凋亡 基因表达 

分 类 号：R363[医药卫生—病理学]