摘要
目的探讨硫化氢供体—硫氢化钠(sodium hydrosulfide,NaHS)对大鼠门静脉高压及内源性一氧化氮(nitric monoxide,NO)/一氧化氮合酶(nitricoxide synthase,NOS)体系的影响。方法将30只健康成年雄性SD大鼠随机分为4组:部分门静脉结扎(partly portal vein ligation,PPVL)组(10只)、PPVL+NaHS组(10只)、假手术组(5只)和正常组(5只)。PPVL组和PPVL+NaHS组行部分门静脉结扎术建立门静脉高压的动物模型。模型制作14天后,分别测定各组大鼠的门静脉压力(PVP)和平均动脉压力(MAP);采用免疫组织化学检测大鼠肝细胞中一氧化氮合酶(NOS2、NOSS)的蛋白水平表达情况,RT-PCR方法检测大鼠肝组织中NOS2和NOS3的mRNA水平的表达情况。结果术后14 d,假手术组和正常组比较,各项检测指标无显著差异,NOS2蛋白及mR-NA水平未见明显表达;NOS3蛋白及mRNA表达水平无显著差异。PPVL组与假手术组比较,PVP明显升高(P<0.05),MAP则下降(P<0.05),PPVL+NaHS组与PPVL组相比较,PVP进一步升高(P<0.05),MAP则进一步降低(P<0.05)。PPVL组和PPVL+NaHS组NOS2在蛋白及mRNA水平均有表达,且后者NOS2蛋白及mRNA表达水平减少(P<0.05)。4组之间NOS3的蛋白及mRNA表达水平则无显著差异。结论H2S参与了门静脉高压的形成与发展,NaHS可以加重门静脉高压,其作用可能与NO/NOS2体系有关。
Objectives To explore the possible impact of hydrogen sulfide donor-NaSH （sodium hydrosulfide ） on experimental portal hypertension （PH） induced by partly portal vein ligation and endogenous nitric oxide/ nitric oxide synthase. Methods Thirty male SD rats were randomly divided into PPVL group （n = 10）, PPVL ＋ NaSH group （n = 10） , sham group （ n = 5） and control group （n = 5）. Rats in PPVL group and PPVL ＋ NaSH group were subjected to the operation of partly portal vein ligation to create an animal model of portal hypertension. Fourteen days later, portal venous pressure （PVP） and systemic mean arterial pressure （MAP） were measured. The expression of nitric oxide synthase （ NOS2, NOS3） protein in hepatic ceils was determined by immunohistochemistry, the expression of nitric oxide synthase （NOS2, NOS3） mRNA was determined by RT-PCR. Results There was no difference between control group and sham group, and we didn＇ t find the expressions of NOS2 protein mRNA. Compared the PPVL group with the sham group, we can find that the PVP in PPVL group was increased （P 〈 0.05 ） , while the MAP was decreased （ P 〈 0.05）. The PVP in the PPVL ＋ NaSH group was increased compared with that in the PPVL group （P 〈 0.05）, and the MAP was decreased too （P 〈 0.05）. We found expressions of NOS2 protein mRNA in both the PPVL group and the PPVL ＋ NaSH group, and the expressions were decreased in the latter group （P 〈 0.05）. Among four groups, the expressions of NOS3 protein mRNA were not changed. Conclusions H2S involves in the pathogenesis of PH, NaSH might promote portal hypertension induced by partly portal vein ligation, and its mechanism might be associated with the changes in endogenous NO/NOS2 pathway.
出处
《胃肠病学和肝病学杂志》
CAS
2007年第6期572-575,共4页
Chinese Journal of Gastroenterology and Hepatology
关键词
硫化氢
门静脉高压
肝
一氧化氮
一氧化氮合酶
Hydrogen sulfide
Portal hypertension
Liver
Nitric oxide
Nitric oxide synthase
