摘要
目的研究缬沙坦对肝纤维化大鼠肝组织血管紧张素转化酶2(ACE2)表达,血管紧张素Ⅱ(AngⅡ)、血管紧张素(1-7)[Ang(1-7)]水平,AngⅡ/Ang(1-7)比值的影响。方法制备复合因素法诱导的大鼠肝纤维化模型,将34只大鼠随机分为3组,正常对照组10只,模型组12只,缬沙坦组12只。造模成功后测定各组大鼠的门静脉压力,并将肝组织进行HE及Masson染色,免疫组化法检测肝组织ACE2的表达,酶联免疫法测定肝匀浆AngⅡ、Ang(1-7)的水平。结果缬沙坦组门静脉压力(PVP)较模型组明显降低(P<0.01),平均动脉压(MAP)、心率(HR)无明显变化;与正常对照组比较,模型组ACE2表达,AngⅡ、Ang(1-7)水平(P<0.01)及AngⅡ/Ang(1-7)比值(P<0.01)均升高;与模型组比较,缬沙坦组ACE2表达及Ang(1-7)水平进一步升高(P<0.05),而AngⅡ无明显变化,AngⅡ/Ang(1-7)比值降低(P<0.05)。结论缬沙坦可降低肝纤维化门静脉压力,其抗肝纤维化,间接降低门脉压力的作用机制可能与该药能够上调ACE2、Ang(1-7)的水平及降低AngⅡ/Ang(1-7)比值有关。
Objective To explore effects of valsartan on expression of angiotensin converting enzyme2 （ACE2）, level of angiotensinⅡ （AngⅡ） and angiotensin（1-7） [Ang（1-7）],ratio of Ang Ⅱ/Ang（1-7） in liver fibrosis rats. Methods Liver fibrosis rats model were induced by compound factors, altogether 8 weeks, 34 rats were randomly divided into three groups （normal group n = 10, model group n=12, treated group n = 12）. Portal pressure was measured after the success of model. Histopathological study of the liver tissue was done with hematoxylin-eosin （HE） and Masson trichrome staining. ACE2 were evaluated by immunohistochemistry. Ang Ⅱ and Ang （1-7） levels were determined by enzyme-linked immunosorbent assay （ELISA）. Results Portal vein pressure （PVP） of valsartan group significantly reduced than model group （P〈0.01）, mean arterial pressure （MAP）, heart rate （HR） had no change; compared with the normal control group, ACE2 expression, AngⅡ , Ang（1-7） level （P〈0.01） and AngⅡ/Ang（1 7） ratio （P〈0.01） were increased in model group; compared with model group, ACE2 expression and Ang（1-7） was further increased in valsartan group （P〈0. 05）, and Ang Ⅱ had no change, AngⅡ/Ang（1 7） ratio were lower （P〈0.05）. Conclusion Effect of valsartan on fibrosis, indirectly reduce portal pressure effects may be associated with increase of ACE2 expression and improvement of Ang（1-7） level,the balance of Ang Ⅱ and Ang（1-7）.
出处
《国际消化病杂志》
CAS
2013年第2期128-131,141,共5页
International Journal of Digestive Diseases
作者简介
通信作者：霍丽娟，Email：mymai15296@163．com
