醛固酮与转化生长因子-β1在心肌纤维化中的作用机制  

Effects and Mechanisms of Aldosterone and Transforming Growth Factor-β1 on Myocardial Fibrosis

作　　者：李林锋[1] 王洪[1] 刘朝晖[1] 罗汛[1] 洪浪[1] 

机构地区：[1]江西省人民医院心内科,南昌330006

出　　处：《实用临床医学（江西）》2012年第10期4-6,9,共4页Practical Clinical Medicine

摘　　要：目的探讨醛固酮与转化生长因子-β1(TGF-β1)在心肌纤维化的作用机制。方法将体外培养的心肌成纤维细胞(CFs)分为对照组、醛固酮组、醛固酮+依普利酮组、依普利酮组及SB431542预处理组。给予相应处理后,ELISA检测TGF-β1水平,RT-PCR检测Smad2、Ⅰ型胶原、Ⅲ型胶原表达。结果与对照组比较,醛固酮处理后,能显著促进TGF-β1分泌,促进Smad2、Ⅰ型胶原、Ⅲ型胶原表达(P<0.01);与醛固酮组比较,醛固酮+依普利酮组TGF-β1分泌、Smad2、Ⅰ型胶原、Ⅲ型胶原表达均明显下降(P<0.01);与醛固酮组比较,SB43l542预处理组抑制Smad2、Ⅰ型胶原和Ⅲ型胶原表达的差异有统计学意义(P<0.01)。结论醛固酮通过激活MR促进CFs细胞TGF-β1分泌,激活Smad2,使Ⅰ型胶原、Ⅲ型胶原表达增加,诱导心肌纤维化。ABSTRACT： Objective To investigate the effects and mechanisms of aldosterone and transforming growth factor-β1 （TGF-β1）on myocardial fibrosis. Methods Cultured cardiac fibroblasts （CFs）were divided into four groups： control group, aldosterone treatment group,eplerenone ptreatment and treatedwith aldosterone treatment group,SB431542 treatwent group. TGF-β1 production was measured by ELISA. The expression of Smad2, collagen type I and collagen type Ⅲ were detected by RT-PCR. Results Compared with control group, aldosterone treatment significantly increased the secretion of TGF-β1 and the expression of Smad2, collagen type I and collagen type Ⅲ （P〈0.01）. Compared with aldosterone treatment group, eplerenone and treated with aldosterone treatment group obviously inhibited the secretion of TGF-β1 and the expression of Smad2, collagen type I and collagen type Ⅲ （P〈0.01）. Moreover, comparedwith aldosterone treatment group SB431542 treatmentgroup also decre- ased the expression of Smad2, collagen type I and collagen type Ⅲ （P〈0.01）. Conclusion Aldosterone can increase the expression of Smad2, collagen type I and collagen type Ⅲ to induce myocardial fibrosis through activating mineralocorticoid receptor antagonists to promote the production of TGF-β1.

关 键 词：醛固酮 转化生长因子-Β1 心肌成纤维细胞 Ⅰ型胶原 Ⅲ型胶原 动物实验 大鼠 

分 类 号：R322[医药卫生—人体解剖和组织胚胎学]