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目的:本实验拟采用转化生长因子(TGF)β1刺激原代大鼠乳鼠心脏成纤维细胞诱导其分化激活,探讨参松养心粉剂在心脏成纤维细胞激活中的作用。方法:体外分离培养大鼠乳鼠心脏成纤维细胞,采用TGFβ1诱导心脏成纤维细胞的激活,同时给予不同浓度的参松养心粉剂处理后,检测各组成纤维细胞增殖、激活程度;采用免疫印迹法探讨其机制。结果:参松养心单独处理成纤维细胞不影响细胞活性;不同浓度的参松养心抑制TGFβ1诱导的心脏成纤维细胞的增殖;50,100μg/ml的参松养心明显抑制细胞的转化激活,抑制促胶原因子的转录水平。免疫印迹结果显示参松养心抑制蛋白激酶B(Akt)、mTOR、GSK3β以及eIF4e的磷酸化。结论:参松养心能够保护TGFβ1诱导的心脏成纤维细胞的增殖、分化以及激活,其主要通过抑制Akt通路发挥抗纤维化的作用。
Objective: In this study, transforming growth factor (TGF) β1 was used to induce primary rat cardiac fibroblasts to induce their differentiation and activation, and to explore the role of Shensong Xinxin powder in cardiac fibroblast activation. Methods: Rat cardiac fibroblasts were isolated and cultured in vitro. TGFβ1 was used to induce the activation of cardiac fibroblasts. At the same time, Shenmai Xinyin powder was used to treat the fibroblasts. The proliferation and activation of fibroblasts were detected by Western blotting Law to explore its mechanism. Results: Shensongyangxin treated fibroblasts alone did not affect the cell viability; Shensongyangxin of different concentrations inhibited the proliferation of cardiac fibroblasts induced by TGFβ1; and Shen-xin-xin of 50,100μg / ml obviously inhibited the transformation and activation of cells, Inhibit transcription factors that promote collagen factor. Immunoblotting results showed that SSC inhibited the phosphorylation of protein kinase B (Akt), mTOR, GSK3β and eIF4e. Conclusion: Shensongyangxin can protect TGFβ1-induced proliferation, differentiation and activation of cardiac fibroblasts, which play an important role in anti-fibrosis by inhibiting Akt pathway.