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作 者:张婕[1] 霍丽娟[1] 武淑君[1,2] 王晋江[1] 贾慧[1]
机构地区:[1]山西医科大学第一医院消化科,太原030001 [2]山西医科大学
出 处:《中华消化病与影像杂志(电子版)》2015年第4期22-25,共4页Chinese Journal of Digestion and Medical Imageology(Electronic Edition)
基 金:山西省卫生厅科研课题计划(201201064)
摘 要:目的观察血管紧张素转化酶抑制剂依那普利、血管紧张素Ⅱ1型受体拮抗剂缬沙坦对肝纤维化大鼠肝组织血管紧张素转化酶2(ACE2)-血管紧张素(1-7)[Ang(1-7)]-Mas轴各组分表达的影响。方法制备四氯化碳诱导的肝纤维化大鼠模型,建模成功后分别给予依那普利、缬沙坦灌胃15 d,将各组大鼠肝组织进行HE及Masson染色,ELISA法测定Ang(1-7)含量,实时PCR技术检测ACE2、Mas mRNA表达,Western印迹法检测ACE2、Mas蛋白表达。结果依那普利、缬沙坦均可改善大鼠肝纤维化程度,增加肝组织Ang(1-7)的含量(t=0.46、6.59,P<0.05),同时还可增加ACE2mRNA(t=5.53、9.29,P<0.05)及其蛋白表达(t=5.77、5.63,P<0.05)、Mas mRNA(t=7.68、6.77,P<0.05)及其蛋白表达(t=2.63、3.89,P<0.05)。结论依那普利、缬沙坦具有良好的抗肝纤维化作用,其机制可能与上调ACE2-Ang(1-7)-Mas轴各组分表达有关。Objective To explore the influence of Enalapril (angiotensin converting enzyme inhibitor) and Valsartan (angiotensin Ⅱ type 1 receptor blocker) on angiotensin converting enzyme 2 (ACE2)/angiotensin (1-7) [ Ang (1-7)]/Mas receptor in rats with liver fibrosis. Methods Rat liver fibrosis models induced by CC14 were made. After modeling success, rats were given 15 days of Enalapril or Valsartan by gastric gavage. Histopathological study of the liver tissue was done with hematoxylin-eosin (HE) and Masson staining. Ang (1-7) level was determined by enzyme-linked immunosorbent assay (ELISA). The mRNA expression and the protein expression of ACE2 and Mas receptor were evaluated by real-time PCR and Western blotting respectively. Results Enalapril and Valsartan attenuated the degree of hepatic fibrosis. Ang( 1-7 ) level ( t = 0.46, 6.59, both P 〈 0.05 ) , ACE mRNA expression level ( t = 5.53, 9.29, both P 〈 0.05 ) and protein expression level (t = 5.53, 9.29, both P 〈 0.05 ) , Mas receptor mRNA expression level (t = 7.68, 6.77, both P 〈 0.05) and protein expression level ( t = 2.63, 3.89, both P 〈 0.05 ) were elevated by Enalapril and Valsartan. Conclusions Enalapril and Valsartan can delay the progression of hepatic fibrosis. The activating of ACE2-Ang (1-7)-Mas axis may be included in the mechanism of Enalapril and Valsartan on anti-hepatic fibrosis.
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