解偶联蛋白-2、PPARγ在梗阻性黄疸及胆道再通大鼠肝脏氧化损伤中的作用  

Roles of uncoupling protein-2 and peroxisome proliferators activated receptors y in liver oxidative injuy of rats with obstructive jaundice and recannalization of biliary tract

作　　者：李蔚[1] 邬善敏[1] 温暖[1] 陈辰[1] 蔡杰[1] 

机构地区：[1]武汉大学人民医院肝胆腔镜外科,430060

出　　处：《腹部外科》2013年第1期65-67,共3页Journal of Abdominal Surgery

基　　金：武汉市科技攻关计划项目（No.201161038342-02）

摘　　要：目的研究解偶联蛋白-2（UCP-2）、过氧化物酶体增殖物激活受体丫（PPART）在梗阻性黄疸及胆道再通大鼠肝脏中的表达与肝功能及超微结构改变的关系。方法将30只雄性Wistar大鼠随机分为3组：假手术组（A组）、梗阻性黄疸1周组（B组）、梗阻性黄疸1周胆道再通1周组（C组），检测各组大鼠血清中直接胆红素（DBIL）、总胆红素（TBIL）和丙氨酸转氨酶（ALT）水平。免疫组织化学法检测UCP-2、PPART蛋白在肝脏中的表达。结果血清DBIL、TBIL、ALT水平：B组明显高于A组，C组明显低于B组。PPAR7的表达：B组明显低于A组，C组较B组明显增强；UCP-2的表达：B组明显强于A组，C组较B组明显减弱。在电镜下可见B组超微结构改变较A组显著，C组超微结构改变较B组明显减轻。结论梗阻性黄疸氧化损伤，造成肝功能及超微结构的改变，解除梗阻有利于肝功能及超微结构的恢复。PPARy可能参与梗阻性黄疸及胆道再通肝脏的氧化与抗氧化反应，UCP-2可能参与肝脏氧化损伤时氧自由基的清除，减轻肝脏氧化损伤。Objective To investigate the relationship between the expression of uncoupling protein-2 （UCP-2） and proliferators activated receptors T （PPART） with the liver function and ultrastructural changes in rats with obstructive jaundice and bile flow restoration rates, and to explore the mechanisms of oxidative injuy in hepatic obstructive jaundice. Methods Thirty healthy male Wistar rats were divided into three groups at random., group A （sham group）, group B （obstructive jaundice one- week group）, group C （obstructive jaundice one-week and recanalization one-week group）. The levels of direct bilirubin （DBIL）, total bilirubin （TBIL） and serum alanine aminotransferase （ALT） were measured. The expression levels of UCP-2 and PPAR7 proteins in hepatic tissues were detected by using immunohistochemistry. Results The levels of serum DBIL, TBIL and ALT in group B were in- creased significantly as compared with group A, and those in group C were lower significantly than in group B. The expression levels of PPAR7 protein in hepatic tissues in group B were lower significantly than in group A, and those in group C were increased significantly as compared with group B. The ex- pression levels of UCP-2 protein in hepatic tissues in group B were increased significantly as compared with group A, and those in group C were lower significantly than in group B. Under an electron microscope, the ultrastructural changes in group B were more significant than in group A, and those in group C were significantly reduced as compared with group B. Conclusion Obstructive jaundice-induced oxidative damage can cause the changes in the liver function and ultrastructures, and relieving obstruction is beneficial to the recovery of the liver function and ultrastruetures. PPAR], may be involved in liver oxidation and oxidation reaction induced by obstructive jaundice and biliary recanalization. UCP-2 may be involved in oxygen free radical removal in liver oxidation damage, reducing liver oxidative damage.

关 键 词：黄疸 阻塞性 胆道 过氧化物酶体增殖物激活受体Γ 

分 类 号：R151.43[医药卫生—营养与食品卫生学]