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作 者:刘维国[1] 郑勇[2] 李文娟[1] 宋丽秀[1] 陈卫刚[2] 刘清华[2] 张宁[2]
机构地区:[1]石河子大学医学院,新疆石河子832000 [2]石河子大学医学院第一附属医院
出 处:《山东医药》2010年第24期39-40,共2页Shandong Medical Journal
基 金:国家自然科学基金资助项目(30850004)
摘 要:目的应用内源性硫化氢(H2S)供体硫氢化钠(NaHS)探讨内源性H2S/胱硫醚-γ-裂解酶(CSE)体系对大鼠肝硬化门静脉压力的影响。方法将32只健康雌性SD大鼠随机分为4组:C组和C+S组采用复合因素法复制肝硬化模型。模型制备52 d后,N+S组和C+S组大鼠腹腔注射NaHS 56μmol/(kg.d),N组和C组腹腔注射同等剂量的生理盐水。1周后分别测定各组大鼠门静脉压力(PVP)及门静脉血浆中H2S含量;采用免疫组织化学方法检测大鼠肝门区门静脉平滑肌细胞中CSE蛋白表达。结果与N组和N+S组相比,C组和C+S组PVP均升高,H2S含量及CSE蛋白表达均降低;与C组相比,C+S组PVP降低,H2S含量及CSE蛋白表达均升高。结论 NaHS作为H2S供体可能具有改善肝硬化大鼠门脉高压的作用,其机制可能与H2S含量及CSE蛋白表达升高有关。Objective To explore the effects of hydrogen sulfide(H2S) donor sodium hydrosulfide(NaHS) on portal vein pressure(PVP) and endogenous H2S/cystathionine-γ-splitting enzyme(CSE) system in rats with portal hypertension induced by heptic cirrhosis.Methods Healthy female SD rats were randomly divided into four groups.Rats in C group and C+S group were made portal hypertension models by injecting carbon tetrachloride(CCL4).Rats in N group and N+NaHS group were fed normally.Then,rats in N+S group and C+S group were injected 56 μmol/(kg·d) NaHS,and rats in N group and C group were injected with the same volume of physiological saline.After one week,PVP and the density of H2S in portal vein blood were measured,then the portal vein and liver tissues were obtained.The expression of CSE in portal vein was measured by using immunohistochemistry method.Results Compared with N group and N+S group,PVP in C group and C+S group increased,the density of H2S and the expression of CSE decreased.Compared with C group,PVP in C+S group decreased,the density of H2S and the expression of CSE increased.Conclusions NaHS could regulate PVP in portal hypertension rats with heptic cirrhosis,its mechanism might be associated with high expression of endogenous H2S/CSE.
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