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作 者:蒋兆彦[1] 韩天权[1] 所广军[2] 袁作彪[1] 姜志宏[1] 商俊[1] 蔡杏兴[1] Gsta Eggertsen Curt Einarsson 张圣道[1]
机构地区:[1]上海第二医科大学附属瑞金医院外科 [2]上海市东方医院外科,200120 [3]瑞典斯德哥尔摩卡罗林斯卡医学院附属乌丁医院消化科
出 处:《外科理论与实践》2005年第1期61-65,共5页Journal of Surgery Concepts & Practice
基 金:国家自然科学基金资助(编号:30271272)
摘 要:目的:本研究旨在测定比较胆石病人与对照组肝脏胆小管侧膜转运蛋白表达差异,以探讨胆石病发生的分子生物学机制。方法:研究包括20例胆囊胆固醇结石病人和11例无胆石症的对照。测定血清胆固醇和甘油三酯、胆汁胆固醇、胆汁酸和磷脂含量,采用Carey表计算胆汁胆固醇饱和指数。实时定量PCR法测定肝脏胆小管侧膜转运蛋白(ABCG5、ABCG8、ABCBll和ABCB4)mRNA的表达量。结果:胆石组血清胆固醇低于对照组(P<0.05)。胆石组胆汁胆固醇摩尔百分比和胆固醇饱和指数较对照组显著升高(P<0.01)。胆石组肝脏胆小管侧膜胆固醇转运蛋白ABCG5和ABCG8表达高于对照组,且后者差异具有统计学显著性(ABCG5:31.44±3.17Vs25.72±3.27,ABCG8:27.53±3.06vs17.81±2.23)。ABCBll和ABCB4表达在两组间差异无显著性。结论:本研究显示,胆石病主要病理生理异常为胆汁胆固醇过饱和,与肝脏胆小管侧膜胆固醇转运蛋白ABCG5和ABCG8的mRNA表达增加有关。Objective To aim at determining mRNA expression of hepatic cannalicular ABC tranporters in patients with cholesterol gallstone disease, to further elucidate the biomolecular pathogenesis of gallstone formation. Methods Twenty patients with cholesterol gallstone (CGS) and 11 controls without gallstones were included in this study. Serum cholesterol, triglycerol and biliary composition were assayed. mRNA expression of ABCG5, ABCG8, ABCB11, ABCB4 genes were determined by real-time PCR. ABCG5/ABCG8, ABCB11 and ABCB4 are hepatic cannalicular transporters for secretion of biliary cholesterol, bile acids and phospholipids. Results Serum cholesterol decreased more evidently in the CGS group than in the control group(P< 0.05),while biliary cholesterol and cholesterol saturation index increased significantly in the CGS group than the control group. The Expression of the hepatic cannalicular cholesterol transporters ABCG5 and ABCG8 was higher in CGS patients than in controls, the difference being statistically significant (ABCG5: 31.44 ±3.17 vs 25.72 ±3.27,ABCG8:27.53±3.06 vs 17.81±2.23). The expression of ABCB11 and ABCB4 did not show much difference between the 2 groups. Conclusions The main pathophysiological profile of patients with cholesterol gallstone disease--the hypersaturation of biliary cholesterol, could be produced by increased expression of hepatic cannalicular cholesterol transporters ABCG5 and ABCG8.
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