黄连素抗心脏纤维化作用及其机制

Berberine inhibit cardiac fibrosis through p38 MAPK pathway

目的观察黄连素对心脏纤维化的影响,探讨其可能机制。方法体外使用转化生长因子-β1(TGF-β1)刺激心脏成纤维细胞,建立心脏纤维化细胞模型。采用不同浓度(10~90μmol/L)黄连素刺激,观察心脏成纤维细胞的活力、胶原Ⅲ和p38 MAPK蛋白表达水平。结果低浓度的TGF-β1可增加心脏成纤维细胞的活力,促进胶原Ⅲ的合成。黄连素呈浓度依赖性地抑制心脏成纤维细胞的活力,降低胶原Ⅲ的合成,促进p38MAPK蛋白磷酸化。结论黄连素可抑制心脏成纤维细胞的增殖和胶原Ⅲ的合成,其机制可能是通过磷酸化p38MAPK蛋白起作用。

Objective To observe the effects of berberine on cardiac fibrosis,and to investigate the possible mechanism. Methods Cardiac fibroblasts were stimulated by TGF- β1 to establish a cell model of cardiac fibrosis. Cardiac fibroblasts were stimulated with different concentrations of berberine before given with TGF- β1. The cell viability,the expression levels of collagen Ⅲ protein and p38 MAPK protein were tested. Results TGF- β1 at low concentration could increase the viability of cardiac fibroblasts and promote the synthesis of collagen Ⅲ. Berberine showed a inhibitive effect on cardiac fibroblast cell viability in a concentration- dependent manner,which reduced the synthesis of collagenⅢ,and promoted the phosphorylation of p38 MAPK protein. Conclusion Berberine can inhibit the proliferation of cardiac fibroblasts and synthesis of collagen Ⅲ via phosphorylation of p38 MAPK proteins.