替米沙坦抑制SHR大鼠心肌Smad2、3蛋白表达及减轻心肌纤维化作用的研究  

Telmisartan inhibited protein Smad2,3 expression and reduced myocardial fibrotic remodeling in SHR

作　　者：曲巍[1] 于波[1] 

机构地区：[1]中国医科大学附属第一临床学院心内科,辽宁沈阳110001

出　　处：《中国当代医药》2010年第25期21-22,34,共3页China Modern Medicine

摘　　要：目的:探讨替米沙坦对自发性高血压大鼠(SHR)心肌纤维化的抑制作用,及心肌Smad2、3蛋白表达的影响。方法:将20只雄性SHR大鼠随机分为两组,分别为替米沙坦组和对照组。分别给予替米沙坦10mg/(kg·d),对照组二甲亚砜1ml/d灌胃,共8周。于实验前、2周、8周,应用尾套法测血压3次。8周后分离血浆检测血管紧张素Ⅱ(AngⅡ)水平。心肌石蜡切片通过免疫组化法测定Smad2、3蛋白和Ⅰ型胶原的表达。结果:灌胃8周后,与对照组相比,替米沙坦组AngⅡ水平明显升高(P<0.05);Smad2、3蛋白和Ⅰ型胶原的表达明显降低(P均<0.05)。结论:替米沙坦能抑制心肌纤维化,这一作用可能部分通过抑制Smad2、3蛋白表达来实现。Objective：To explore the effects of telmisartan on myocardical fibrotic remodeling and involvement of protein Smad2,3 expression.Methods：Twenty male SHR were randomly divided into 2 groups,telmisartan group and comparative group.Telmisartan group were poured telmisartan 10 mg/（kg·d）;comparative group were poured dimethyl sulfoxide 1 ml/d in stomach.Before,after two weeks and 8 weeks treatment,the blood pressure were measured by tail-sleeve method.At week 8,the levels of AngⅡ in plasma were measured by radioimmunoassay kit.After week 8,the protein levels of Smad2,3 and collagen Ⅰ were assayed by angiography and histomorphometric analysis.Results：Following 8 weeks treatment,telmisartan group displayed a significant elevation in the levels of Ang Ⅱ,P〈0.05,and reduction in Smad2,3 and collagen Ⅰ（P〈0.05 respectively）.Conclusion：Telmisartan attenuates myocardical collagen synthesis in SHR possibly through downregulating the expression of Smad2,3.

关 键 词：替米沙坦 心肌纤维化 Smad2、3蛋白 

分 类 号：R332[医药卫生—人体生理学]