通心络通过调节TGF-β1/Smads通路抑制高糖处理大鼠心肌成纤维细胞功能的机制研究

Study on the Mechanism of Tongxinluo Inhibiting the Function of Myocardial Fibroblasts Treated with High Glucose by Regulating TGF-β1/Smads Pathway

目的 观察通心络抑制高糖处理的大鼠心肌成纤维细胞功能的作用及可能的机制。方法 大鼠心肌成纤维细胞分为对照组和模型组,通心络分为低、中、高剂量组,MTT法检测各组细胞的增殖和活力,酶联免疫检测Ⅰ、Ⅲ型胶原蛋白及TGF-β1蛋白表达水平,免疫印迹检测phopho-Smad2、phopho-Smad3,Smad7蛋白表达水平。结果 模型组的细胞增殖和活力明显高于对照组,Ⅰ、Ⅲ型胶原蛋白、TGF-β1蛋白表达水平显著升高;与对照组比较,模型组的phospho-Smad2、phospho-Smad3蛋白表达水平明显升高,而通心络各组上述异常指标均得到改善,通心络各组Smad7蛋白表达水平明显高于模型组。结论 通心络能够抑制成纤维细胞的增殖和活力,从而抑制了Ⅰ、Ⅲ型胶原的活性,减少了Ⅰ、Ⅲ型胶原的分泌,通心络的上述作用可能是通过对TGF-β1/Smads通路的活化进行调节来实现的。

Objective To observe the inhibitory effect of Tongxinluo on the function of myocardial fibroblasts treated with high glucose and its possible mechanism.Methods Rat cardiac fibroblasts were divided into control group,model group and Tongxinluo experimental groups with low,medium and high dose.The proliferation and activity of each group were detected by MTT,and the expression levels of type I,III collagen and TGF-β1 protein in each group were detected by enzyme-linked immunoassay.The protein expression levels of Phopho-Smad 2,Phopho-Smad 3 and Smad 7 were detected by western blot.Results The cell proliferation and activity of model group were significantly higher than those of control group,and the expression levels of type I and III collagen and TGF-β1 protein were significantly increased;compared with the control group,the expression levels of phospho-smad 2 and phospho-smad 3 protein in the model group were significantly increased,while the above abnormal indexes in Tongxinluo group were improved.At the same time,the expression level of Smad 7 protein in Tongxinluo group was significantly higher than that in the model group.Conclusion Tongxinluo can significantly inhibit the proliferation and vitality of fibroblasts,and then inhibit the activity of type I,III collagen and reduce the secretion of type I,III collagen collagen.The above effects of Tongxinluo may be realized by regulating the activation of TGF-β1/Smads pathway.