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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 investigate the regulatory mechanism of liver damage in obstructive jaundice. Methods The apoptosis status and the expression of apoptosis-related genes bcl 2 and bax in liver tissues of 40 obstructive jaundice rats were detected by TUNEL and immunohistochemistry . Results After the common bile duct was ligated, the apoptosis increased with the ligation time. The apoptosis peaked at 14 days after ligation and the apoptotic index (AI) reached 5 8.23 ± 1.58 (P <0. .0 5). In the process of obstructive jaundice, the stronger the expression of bcl 2 protein, the weaker the expression of bax protein, the less AI. Conclusion Both bcl 2 and bax proteins are involved in the regulation of apoptosis in hepatic tissues of obstructive jaundice.