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目的 探讨阻塞性黄疸大鼠肝组织损害的机制．方法 用末端脱氧核苷酸转移酶（ＴｄＴ） 介导的ｄＵＴＰ 缺口末端标记技术（ＴＵＮＥＬ） 和免疫组织化学方法检测阻塞性黄疸大鼠肝脏组织细胞凋亡状态及凋亡相关基因ｂｃｌ２ 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１４ ｄ 后细胞凋亡达高峰，凋亡指数（ＡＩ） 达５８－２３ ±１－５８ ，各组ＡＩ差异有显著性意义（ Ｐ＜ ０－０５） ． 在阻塞性黄疸过程中，ｂｃｌ２ 蛋白表达越强，ＡＩ就越少．结论 ｂｃｌ２ 蛋白参与了阻塞性黄疸肝组织中细胞凋亡的调节，并在阻塞性黄疸肝损害的发生和发展中起重要作用．
Objective To investigate the mechanism of liver damage in obstructive jaundice rats. Methods TdT-mediated dUTP nick end labeling (TUNEL) and immunohistochemistry were used to detect the apoptotic status and the expression of bcl-2 in liver tissue of obstructive jaundice rats . Results After the common bile duct was ligated, the apoptosis increased with the prolongation of the ligation time. After 14 days of ligation, the apoptosis peaked and the apoptotic index (AI) reached 58-23 ± 1-58. There was a significant difference in AI among all groups P <0-05). In the process of obstructive jaundice, the stronger the expression of bcl 2 protein, the less AI. Conclusion bcl 2 protein is involved in the regulation of apoptosis in hepatic tissue of obstructive jaundice and plays an important role in the occurrence and development of hepatic damage in obstructive jaundice.