摘要
目的研究梗阻性黄疸(简称:梗黄)状态下大鼠肝脏细胞损害的发展规律及机制,探讨维拉帕米对肝细胞保护作用。方法使用生化、免疫组化、末端脱氧核甘酸介导生物素标记(TUNEL)技术和HE染色测量不同组别、不同梗黄时间大鼠肝脏细胞的坏死及凋亡指数(AI)Bax蛋白表达和活性氧(ROS)水平,并进行统计分析。结果随着胆总管结扎时间的延长,单纯梗黄组大鼠(G1)肝脏细胞凋亡和坏死程度逐渐加重,ROS水平持续升高,Bax蛋白表达进行性升高。A1与ROS水平、Bax蛋白表达变化呈正相关。维拉帕米治疗组(G2)呈现相似变化,但各时相点上,细胞坏死及A1均较G1轻。组间ROS水平和Bax蛋白表达差异具有显著性(P<0.05)。结论维拉帕米对梗黄肝细胞损害有明显保护作用。纠正钙稳态失调可能是其抑制细胞凋亡的重要途径。
Objective To explore the mechanism of hepatic damage and the protection of in the liver of obstructive jaundice rats（OJ）.Methods Terminal-deoxynucleotidyl medicated nick end labeling（TUNEL）, HE, hiochemical and immunhischemical methods were used to measure hepatic necrosis, hepatic apoptosis, ROS and the expression of Bax in liver in different rat groups at certain timepoints. Results The longer the time of OJ in the rats,the heavier hepatic necrosis and hepatic apoptois.After common bile duct（CBD） Ligation. The expression of Bax and ROS increased in rats liver gradually. Less hepatic damage occured in the OJ rats treated with at any time point（ P 〈 0.05） .Conclusion exerted great protection effect on the liver of rats with obstructive jaundice and the mechanism of protection may be realized through regulating the calcium hemostasis.
出处
《黑龙江医学》
2007年第5期350-352,共3页
Heilongjiang Medical Journal
