摘要
目的观察70%门静脉分支高位结扎后大鼠肝组织细胞凋亡及相关基因Bax,Bcl-2的表达,以探讨肝细胞凋亡的发生机制。方法Wistar大鼠60只,随机分成假手术对照组(n=30)和门静脉结扎组(n=30)。观察术后第12小时和第1,2,3,7,14天的肝脏大体结构和血浆转氨酶的变化。用细胞凋亡原位末端标记技术(TUNEL)对结扎侧肝细胞凋亡进行定量分析,光学显微镜下观察未结扎侧肝细胞的增殖情况,采用逆转录-多聚酶链反应(RT-PCR)检测肝脏组织中Bax和Bcl-2 mRNA的表达。结果70%门静脉分支高位结扎后,结扎侧肝叶以细胞凋亡的方式呈进行性萎缩变小,对侧则以有丝分裂的方式成比例地代偿性增生。全肝的总质量维持恒定,肝脏功能基本保持正常。结扎侧肝组织中以Bax mRNA的升高为主,而未结扎侧肝组织中以Bcl-2 mRNA的升高为主。结论近70%门静脉分支高位结扎后,结扎侧肝脏由于Bax mRNA表达升高引起肝细胞大量凋亡,未结扎侧由于Bcl-2 mRNA表达升高引起肝细胞增殖,在维持全肝的质量和功能中具有重要意义。
Objective To observe apoptosis of hepatocytes in rats after ligation of 70% portal branch and expressions of apoptotic related genes Bax and Bcl-2,and to study the mechanism of hepatocytic apoptosis. Methods Sixty Wistar rats were randomily divided into control group（n=30）and portal branch ligation group（n=30）. Animals were killed at the 12th hour,on the 1st, 3rd, 7th and 14th day,respectively. To determine the contents of plasma ALT,the degree of hepatic regeneration and apoptosis were observed under microscope and TUNEL. Bax and Bcl-2 gene expression in liver tissue were assessed by RT-PCR. Results Hepatic lobe at the ligated side atrophied and diminished progressively due to apoptosis after ligation of 70% portal branch, whereas the lobes at the opposite side were underwent compensatory regeneration through mitosis, the total liver quality and plasma ALT level were main- tained proportionately invariabienes throughout the experiment. Bax gene expression increased in the ligated lobe and Bcl-2 gene expression increased in the unligated lobes. Conclusion After ligation of 70% branches of the portal the ligated lobes atrophies through hepatocytes apoptosis caused by Bax gene overexpression,whereas the perfused lobes undergo compensatory regeneration through mitosis because of Bcl-2 gene overexpression,which play important roles in maintaining total liver weight and function.
出处
《肝胆胰外科杂志》
CAS
2007年第3期168-170,173,共4页
Journal of Hepatopancreatobiliary Surgery
基金
温州市科技局资助项目(2005-208)
关键词
门静脉
结扎术
肝细胞
凋亡
增殖
基因表达
大鼠
portal vein
ligation
hepatocytes
apoptosis
regeneration
gene expression
rat
