中文摘要：

目的检测过氧化体增殖剂激活受体（peroxisome proliferators—activated receptors，PPARs）、超氧化物歧化酶（superoxide dismutase，SOD）及核因子-κB（Nuclear factor-κB，NF-κB）在梗阻性黄疸大鼠肝脏中的表达，明确其在梗阻性黄疸肝脏损害中的作用及意义。方法检测血清总胆红素（total bilirubin，TB）、直接胆红素（direct bilirubin，DB）和谷丙转氨酶（alanine aminotransferase，ALT）。肝脏组织行HE病理切片检查。肝脏组织匀浆后检测组织中总SOD和CuZb-SOD活力，RT—PCR方法检测PPARs在肝脏中的mRNA，以免疫组织化学方法检测PPARs及NF-κB在肝脏中的表达。结果胆道结扎组（bile duct ligation，BDL）血清TB、DB及ALT明显增高（P〈0．01）。肝组织中总SOD和CuZn—SOD活力胆道结扎组较假手术组明显减低（P〈0．01）。除7d组的PPARβ外，胆道结扎组PPARs在肝脏中的mRNA表达较对照组明显下调（P〈0．01），且19d组较7d组显著；PPARs在肝脏组织表达明显下降（P〈0．01）；NF-κBp65蛋白在胆道结扎组激活并出现核移位，19d组较7d组更加显著。胆道结扎组大鼠肝脏总SOD活力与PPARs蛋白表达呈显著正相关（P〈0．01），而NF-κBp65蛋白表达与PPARs蛋白表达呈显著负相关（P〈0．01）。结论PPARs在梗黄大鼠肝脏中，基因和蛋白水平均受到抑制，且随梗阻时间延长而加重；PPARs可能为SOD及NF-κB的上游调控因子，在梗黄肝脏损害中发挥作用。

英文摘要：

Objective To determine the expression of peroxisome proliferators-activated receptors （PPARs）, nuclear factor -κB （NF-κB） and activity of superoxide dismutase （SOD） in rats with obstructive jaundice induced by bile duct ligation （BDL） and elucidate the molecular regulation mechanisms of hepatic injury due to obstructive jaundice. Methods All rats were sacrificed on the 7th day and 19th day after BDL and blood and liver tissue samples were obtained. SOD enzyme activity was detected by SOD kit. RT PCR was performed to determine the mRNA expression of PPARs in all groups. The detection of PPARs protein and activation of NF-κB were performed using an immunohistochemical method. Results The activities of normal SOD and CuZn-SOD were decreased compared to the sham group （P〈0.01）, and the decrease on 19th day after BDL were more significant. The level of PPARs expression in the BDL groups liver except the PPARβ in the BDL 7th group was reduced compared to the sham group （P〈0.01） , and the level on the 19th day after BDL were more significantly reduced. PPARs protein expression was significantly inhibited （P〈 0.01） in the sham group. SOD in BDL groups had significant positive correlation as compared with PPARs protein expression （P〈0.01）, but NF-κBp65 protein expression had significant negative correlation as compared with PPARs protein expression （P〈0.01）. Conclusion PPARs are inhibited in expression level, and this inhibition becomes more significant as the pathological process progresses. PPARs might be key regulatory factors for SOD and NF-κB. The low expression of PPARs might be one of the important molecular mechanisms in liver injury due to obstructive jaundice.