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.
出处
《实用临床医学（江西）》
CAS
2012年第10期4-6,9,共4页
Practical Clinical Medicine
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
aldosterone
transforming growth factor-β1
cardiac fibroblasts
collagen type I
collagen type m
animals, laboratory experimen
rats
