目的:探讨黄芪甲苷(ASIV)对脂多糖(LPS)诱导心肌细胞肥大的保护作用及机制。方法:利用体外培养模型,以脂多糖1 mg/L诱导心肌细胞肥大,观察不同剂量黄芪甲苷(12.5、25、50 mg/ml)及环孢菌素A(CsA)对脂多糖诱导的心肌肥大的抑制作用。用考马斯亮蓝法测心肌细胞蛋白质含量;消化分离法及计算机图像分析系统检测心肌细胞体积;倒置荧光显微镜下观察细胞形态大小;电泳法测定钙调磷酸酶(CaN)的表达。结果:与正常对照组相比,脂多糖模型组使心肌细胞总蛋白质含量增加,细胞体积增大,钙调磷酸酶表达增加。与模型组相比,黄芪甲苷(25、50 mg/ml)可有效改善脂多糖诱导的心肌细胞肥大,抑制钙调磷酸酶表达增加,并呈一定的剂量依赖性。结论:黄芪甲苷可通过抑制钙调磷酸酶信号通路抑制脂多糖诱导的心肌细胞肥大。 Objective: To investigate the protective effect of astragaloside IV (ASIV) on cardiomyocyte hypertrophy induced by lipopolysaccharide (LPS) and its mechanism. Methods: Myocardial cell hypertrophy was induced by lipopolysaccharide (1 mg / L) in vitro and the effects of different doses of Astragaloside (12.5,25,50 mg / ml) and cyclosporin A (CsA) Hypertrophy inhibitory effect. The protein content of cardiomyocytes was measured by Coomassie brilliant blue method. The volume of cardiomyocytes was detected by digestion and computer image analysis system. The morphology of cells was observed under inverted fluorescence microscope. The expression of calcineurin (CaN) was detected by electrophoresis. Results: Compared with the normal control group, the lipopolysaccharide model group increased the total protein content of cardiomyocytes, increased the cell volume and increased the expression of calcineurin. Compared with the model group, Astragaloside (25,50 mg / ml) could effectively improve lipopolysaccharide-induced cardiomyocyte hypertrophy and inhibit the increase of calcineurin expression in a dose-dependent manner. Conclusion: Astragaloside IV can inhibit lipopolysaccharide - induced cardiomyocyte hypertrophy by inhibiting calcineurin signaling pathway.