中文摘要：

目的：探讨罗布麻提取物对血管紧张素Ⅱ（AngⅡ）诱导的大鼠心肌纤维化模型中ERK通路的影响,并初步探索罗布麻提取物抗心肌纤维化机制。方法：采用1×10-6 mol.L-1 AngⅡ诱导大鼠心肌成纤维细胞复制心肌纤维化模型,细胞分为正常对照组、AngⅡ组、缬沙坦治疗组1×10-6 mg.L-1）及罗布麻提取物高剂量组（0.8mol.L-1）、中剂量组（0.4 mol.L-1）、低剂量组（0.2 mol.L-1）。通过对羟脯氨酸及Ⅰ、Ⅲ型胶原（ColⅠ、ColⅢ）的检测鉴定模型的成功复制,RT-PCR及Western blotting方法检测raf、ERK、c-fos mRNA及ERK蛋白在各组细胞中的表达量。结果：成功建立AngⅡ诱导的心肌纤维化模型。与AngⅡ组比较,不同剂量罗布麻提取物组羟脯氨酸及ColⅠ、ColⅢ的表达量均下调（P〈0.05或P〈0.01）;RT-PCR及Western blotting检测发现,罗布麻提取物不同剂量组的raf、ERK、c-fos mRNA及ERK蛋白表达量较AngⅡ组降低（P〈0.05或P〈0.01）。结论：ERK信号通路在罗布麻提取物调控心肌纤维化发生和发展的过程中发挥重要作用。

英文摘要：

Objective To investigate the influence of apocynum venetum extract（AVE） on angiotensin Ang Ⅱ-induced myocardial fibrosis in rats and to clarify its mechanism of anti-myocardial fibrosis.Methods The rat cardiac fibroblasts were pretreated with Ang Ⅱ,and then treated with different concentrations of AVE（0.8,0.4 and 0.2 mol·L-1） or valsartan 10-6 mg·L-1.The expressions of hydroxyproline,collagen Ⅰ,Ⅲ（ColⅠ,ColⅢ） were detected to identify the model of myocardial fibrosis.The expressions of raf,ERK and c-fos mRNA were determined by RT-PCR.The expression of ERK protein was measured by Western blotting.Results The models of myocardial fibrosis were established successfully.Compared with AngⅡ group,the over expressions of hydroxyproline,ColⅠ and ColⅢ in AVE groups were significantly decreased（P〈0.05 or P〈0.01）.Compared with control group,the expressions of raf,ERK and c-fos were increased obviously in Ang Ⅱ group;compared with Ang Ⅱ group,the expressions of raf,ERK and c-fos mRNA and ERK protein in AVE groups were decreased（P〈0.05 or P〈0.01）.Conclusion ERK pathway plays an important role in the occurrence and development of mycardiol fibrosis regulated by AVE.