内源性硫化氢对肝硬化大鼠肝细胞凋亡的影响  

Effect of endogenous hydrogen sulfide on apoptosis of cirrhosis rat liver cells

作　　者：刘浩[1] 郑勇[2] 陈卫刚[2] 赵瑾[3] 李睿[2] 张宁[2] 刘芳[2] 阎继攀[1] 

机构地区：[1]石河子大学医学院,新疆维吾尔自治区石河子市832002 [2]石河子大学医学院第一附属医院消化内科,新疆维吾尔自治区石河子市832008 [3]石河子大学医学院第一附属医院病理科,新疆维吾尔自治区石河子市832008

出　　处：《世界华人消化杂志》2012年第8期670-674,共5页World Chinese Journal of Digestology

基　　金：国家自然科学基金资助项目;No.30850004;石河子大学研究生创新基金资助项目;No.YJCX2010-Z11~~

摘　　要：目的:探讨硫化氢(hydrogen sulfide,H2S)代谢酶抑制剂对肝硬化大鼠肝细胞凋亡的影响,进一步了解内源性H2S在大鼠肝硬化过程中发挥保护性作用的机制.方法:将40只♀SD大鼠分为4组,正常对照组(N组),正常对照组+炔丙基甘氨酸(PPG)组(P组),肝硬化组(H组),肝硬化+PPG组(PH组).H组、PH组利用CCL4复合因素法复制肝硬化大鼠模型,P组和PH组给予腹腔注射PPG(30mg/kg·d)减少大鼠体内H2S含量;N组和H组腹腔注射同等剂量的生理盐水.免疫组织化学法检测大鼠肝组织中细胞胱硫醚γ裂解酶(CSE)的表达,Tunel法检测大鼠肝组织中肝细胞的凋亡,Western-blot法检测大鼠肝组织中凋亡相关蛋白Bax、Bcl-2的表达.结果:H组与N组相比,凋亡指数(AI)明显升高(P=0.000),凋亡促进蛋白Bax表达升高(P=0.001);PH组与H组相比,CSE表达降低(P=0.029),AI明显升高(P=0.000),Bax表达增高(P=0.021),差异均具有统计学意义.Bcl-2在各组间的表达无显著性差异(P=0.742).结论:H2S代谢酶抑制剂可促进肝硬化大鼠肝细胞的凋亡,其作用机制可能与其调节Bax的表达有关.AIM： To explore the effect of a metabolic inhibitor of hydrogen sulfide on apoptosis of liver cells in rats with cirrhosis, and to explore the mechanism underlying the protective effect of hydrogen sulfide against cirrhosis. METHODS： Forty female SD rats were randomly divided into four groups： normal controls （group N）, normal controls treated with propargylglycine （PPG） （group P）, cirrhotic rats （group H）, and cirrhotic rats treated with PPG （group PH）. Rats in groups H and PH were subjected to induction of cirrhosis by injecting carbon tetrachloride （CCl 4 ）. Rats in groups P and PH were injected with PPG （30 mg/kg·d） to decrease the content of hydrogen sulfide in the liver. Rats in groups N and H were injected with equal volume of normal saline. The distribution of cystathionine-γ-lyase （CSE） in the liver was examined by immunohistochemistry. The apoptosis of liver cells was detected by TUNEL assay. The expression of Bax and Bcl-2 in liver cells was detected by Western blot. RESULTS： Compared to group N, apoptosis index （AI） significantly increased （P = 0.000） and expression of Bax was significantly up-regulated （P = 0.001） in group H. Compared to group H, AI and expression of Bax significantly increased （P = 0.000, 0.021）, and CSE decreased （P = 0.029） in group PH. CONCLUSION： Inhibition of hydrogen sulfide promotes apoptosis of liver cells in rats with cirrhosis possibly by regulating the expression of Bax.

关 键 词：硫化氢 肝硬化 BAX BCL-2 凋亡 

分 类 号：R575.2[医药卫生—消化系统]