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Fas/FasL、Bcl-2基因在急性阻塞性黄疸肝细胞中的表达及意义

The Expression of Fas/FasL,Bcl-2 Gene in Hepatocyte During Acute Obstructive Jaundice
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摘要 目的 研究Fas/FasL、Bcl- 2基因在急性阻塞性黄疸肝细胞凋亡中的表达情况。方法 SD大鼠 30只 ,随机分为 3组。A组为假手术组 ,B、C组为实验组 ,结扎胆总管 ,B组饲养 7d ,C组饲养 14d。每组动物处置后观察肝细胞凋亡现象 ,检测肝细胞凋亡率和Fas、FasL、Bcl- 2基因的表达情况。结果  (1)电镜观察到B、C组肝细胞有典型的凋亡现象。 (2 )各组间的肝细胞凋亡率比较有统计学意义 (P <0 .0 5 )。 (3)各组大鼠肝细胞中Fas均有阳性表达 ,阳性率比较无显著差异 (P >0 .0 5 ) ;各组FasL、Bcl- 2阳性率有显著差异 (P <0 .0 5 ) ,C组高于B组。结论  (1)肝细胞凋亡率的升高是导致阻塞性黄疸肝损伤的一个重要机制。 (2 )Fas/FasL系统是阻塞性黄疸肝细胞凋亡的一个重要途径。 (3)Bcl- Objective To investigate the expression of Fas/FasL and Bcl-2 gene in hepatocytes during obstructive jaundice. Methods Thirty SD rats were divided into 3 groups randomly and equally. Group A was sham operation group. Group B, C were made for the experimental models of obstructive jaundice with ligation of the bile duct. The rats in group A, B were sacrificed after feeding for 7 days and the ones in group C were sacrificed after feeding for 14 days. The hepatocyte apoptosis was observed, and the apoptosis rate and the expression of Fas, FasL, Bcl-2 were examined. Results (1)The classic phenomenon of hepatocyte apoptosis was obvious in the liver tissue in BDL rats. (2)The apoptosis rate was significantly different among these groups ( P <0.05). (3)There was positive expression of Fas in the hepatocytes in every group , and there was no significant difference for positivity rate( P >0.05). The positivity rate of FasL and Bcl-2 was significantly different among these groups ( P <0.05), and positivity rate in group C was higher than that in group B. Conclusion (1)The hepatocyte apoptosis in BDL rats is an important cause for liver injury. (2) Fas/FasL system plays a predominant role in the hepatocyte apoptosis of BDL rats. (3) The positive expression of Bcl-2 gene is a kind of adaptive ability of hepatocyte to resist apoptosis induced by toxic bile acid.
出处 《苏州大学学报(医学版)》 CAS 2003年第5期522-524,共3页 Suzhou University Journal of Medical Science
关键词 阻塞性黄疸 肝损伤 凋亡 FAS FASL BEL-2 obstructive jaundice liver injury apoptosis Fas FasL Bcl-2
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