芦丁对心肌纤维化大鼠ColⅠ、ColⅢ、TGF-β1的调控作用

Effects of rutin on the regulation of ColⅠ,Col Ⅲ, TGF-β1 expression in myocardial fibrosis rats

目的研究芦丁对心肌纤维化大鼠ColⅠ、ColⅢ、TGF-β1的调控作用及其机制的变化。方法出生1 d Wistar大鼠6只,将大鼠分别贴上序号1~6,1、2号大鼠为模型组(用含有血管紧张素Ⅱ(AngⅡ)(9~5 mol/L)培养液来培养细胞);3、4号大鼠为芦丁组(在模型组的培养条件下加入芦丁,配成含量是5 mg/L培养细胞液);5、6号大鼠为正常对照组(用含有16%胎牛血清DMEM的培养液培养)。用ELISA法检测培养上清中ColⅠ和ColⅢ的含量和Western blotting法检测转化生长因子-β1(TGF-β1)蛋白表达。结果 ELISA检测显示,AngⅡ作用心肌纤维细胞24 h后,模型组细胞培养的上清液内ColⅢ和ColⅠ的含量较对照组明显上升(P<0.01);经芦丁治疗后,ColⅢ和ColⅠ的含量较模型组均明显下降(P<0.01)。Western blotting结果显示,使用AngⅡ激发心肌纤维细胞24 h以后,模型组的TGF-β1蛋白表达较对照组显著上升(P<0.01),经芦丁培养后,TGF-β1蛋白较模型组显著下降(P<0.01)。结论芦丁可以调控ColⅠ、ColⅢ、TGF-β1的蛋白表达,从而控制大鼠心肌纤维化。

Objective To study the effects of rutin on Col I,Col Ⅲ and transforming growth factor- β1（TGF- β1）expression in myocardial fibrosis rats and its mechanism. Methods Six Wistar rats were randomly numbered as 1 to 6;1and 2 used as model group M,with an average weight of（0.462±0.132）kg;3 and 4 were used as rutin group R,with an average weight of（0.446±0.151）kg;5 and 6 used as normal control group C,with an average weight（0.451±0.166）kg.Heart cells were collected and treated with angiotensin II 9-5 mol/L for model group,and with angiotensin II 9-5 mol/L plus rutin 5 mg/L for rutin group,and normal control group was untreated. The contents of Col Ⅰ and Col Ⅲ in culture supernatant were detected by ELISA method,and the expression of TGF- β1 protein was detected by Western blotting.Results The concentration of Col Ⅲ and Col Ⅰ in the culture supernatant of group M increased significantly（P〈0.01）24 h after myocardial cells were treated with AngⅡ（P〈0.01）. The contents of Col Ⅲ and Col Ⅰ in group R were significantly decreased（P〈0.01）. Western blotting showed that the expression of TGF-β1 in group M was significantly higher than that in group C（P〈0.01）24 h after stimulation with AngⅡ. Compared with group M,The expression of TGF-β1 protein in group R was significantly decreased（P〈0.01）. Conclusion Rutin could regulate Col Ⅰ,Col III and TGF-β1 protein expression,thereby controlling myocardial fibrosis in rats.