内源性H_2S对大鼠实验性肝硬化门脉高压的影响  

Endogenous hydrogen sulfide attenuates portal hypertension in rats with experimental hepatic cirrhosis

作　　者：陈卫刚[1] 郑勇[1] 宋丽秀[1] 刘维国[1] 李文娟[1] 刘清华[1] 张宁[1] 齐翠花[1] 

机构地区：[1]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832000

出　　处：《世界华人消化杂志》2011年第5期467-471,共5页World Chinese Journal of Digestology

基　　金：国家自然科学基金资助项目;No.30850004~~

摘　　要：目的:研究新型气体信号分子硫化氢(hydrogen sulfide,H2S)对大鼠肝硬化门脉高压的影响及其调节机制.方法:对照组(8只),肝硬化(Cirrhosis,C)组(8只),C+NaHS(C+S)组(8只),C+左旋硝基精氨酸甲酯(L-NAME)+锌原卟啉(ZnPP)(C+L+Zn)组(8只),C+NaHS+L-NAME+ZnPP(C+S+L+Zn)组(8只).插管法测定各组大鼠门静脉压力(PVP),同时测定血浆中H2S、NO、CO含量;Westernblot技术检测各组大鼠肝组织中CSE、iNOS、HO-1蛋白表达情况.结果:与对照组相比,其他各组大鼠PVP显著升高(均P<0.05),血浆中H2S、NO、CO含量及CSE、iNOS、HO-1蛋白表达差别均有统计学意义(H2S:134.49μmol/L±12.25μmol/L,151.19μmol/L±8.75μmol/L,160.82μmol/L±6.79μmol/L,170.58μmol/L±4.38μmol/Lvs180.33μmol/L±11.71μmol/L;NO:160.12μmol/L±4.18μmol/L,129.25μmol/L±3.09μmol/L,100.24μmol/L±3.80μmol/L,90.23μmol/L±2.87μmol/Lvs81.11μmol/L±2.91μmol/L;CO:111.12μmol/L±2.25μmol/L,100.43μmol/L±1.42μmol/L,83.72μmol/L±1.78μmol/L,77.58μmol/L±8.17μmol/Lvs70.51μmol/L±3.09μmol/L;CSE:121.72±1.61,150.26±1.04,142.79±1.13,157.28±0.90vs159.30±1.37;HO-1:155.79±1.29,149.89±1.63,139.88±1.73,135.49±1.21vs125.44±0.93;iNOS:165.69±1.17,160.68±1.28,150.66±1.42,145.55±1.04vs135.22±0.54,均P<0.05).结论:内源性H2S/CSE体系在缓解肝硬化门脉高压中发挥着重要的调节作用,其机制可能与NO/NOS、CO/HO-1体系的改变有关.AIM：To investigate the effect of endogenous hydrogen sulfide（H2S） on portal vein pressure in rats with experimental hepatic cirrhosis-induced portal hypertension and to explore mechanisms involved.METHODS：Forty Sprague-Dawley rats were randomly and equally divided into control group,cirrhosis group,sodium hydrogen sulfide（NaHS） group,L-arginine methyl ester（L-NAME） plus zinc protoporphyrin（ZnPP） group,and NaHS plus L-NAME plus ZnPP group.After treatment,portal vein pressure and the levels of H2S,NO,and CO in portal vein blood were measured,and the expression of cystathionine γ-lyase（CSE）,nitric oxide synthase（NOS）,and heme oxygenase（HO-l） in liver tissue was determined by Western blot.RESULTS：Compared with the control group,portal pressure was significantly elevated（all P 0.05） and the levels of plasma H2S,NO,CO and hepatic CSE,iNOS,and HO-1 showed statistically signif icant differences in the other groups（H2S：134.49 μmol/L ± 12.25 μmol/L,151.19 μmol/L ± 8.75 μmol/L,160.82 μmol/L ± 6.79 μmol/L,170.58 μmol/L ± 4.38 μmol/L vs 180.33 μmol/L ± 11.71 μmol/L;NO：160.12 μmol/L ± 4.18 μmol/L,129.25 μmol/L ± 3.09 μmol/L,100.24 μmol/L ± 3.80 μmol/L,90.23 μmol/L ± 2.87 μmol/L vs 81.11 μmol/L ± 2.91 μmol/L;CO：111.12 μmol/L ± 2.25 μmol/L,100.43 μmol/L ± 1.42 μmol/L,83.72 μmol/L ± 1.78 μmol/L,77.58 μmol/L ± 8.17 μmol/L vs 70.51 μmol/L ± 3.09 μmol/L;CSE：121.72 ± 1.61,150.26 ± 1.04,142.79 ± 1.13,157.28 ± 0.90 vs 159.30 ± 1.37;HO-1：155.79 ± 1.29,149.89 ± 1.63,139.88 ± 1.73,135.49 ± 1.21 vs 125.44 ± 0.93;iNOS：165.69 ± 1.17,160.68 ± 1.28,150.66 ± 1.42,145.55 ± 1.04 vs 135.22 ± 0.54,all P 0.05）.CONCLUSION：Endogenous H2S/CSE can regulate portal hypertension in rats with experimental hepatic cirrhosis perhaps via mechanisms associated with the changes in the NO/NOS and CO/HO-1 pathways.

关 键 词：肝硬化 门静脉高压 硫化氢 门静脉压力 一氧化碳合酶 一氧化氮合酶 

分 类 号：R575.2[医药卫生—消化系统]