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目的:探讨黄芪甲苷对苯肾上腺素(PE)诱导心肌肥大的抑制作用及其机制。方法:利用体外培养模型,以苯肾上腺素10μmol/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)及钙调神经磷酸酶(CaN)抑制剂环孢菌素A(CsA)1μmol/L对苯肾上腺素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;倒置相差显微镜观察细胞形态;采用Till阳离子测定系统以Fura-2/AM为荧光探针,观察胞内[Ca2+]i瞬间变化;Werstern印迹法测定CaN表达。结果:与正常对照组相比,苯肾上腺素使心肌细胞总蛋白质含量增加56.2%,细胞体积增大79.6%,心肌细胞内[Ca2+]i静息水平明显升高,CaN表达增加,黄芪甲苷(25,50 mg/ml)可有效改善苯肾上腺素诱导的心肌细胞肥大,抑制[Ca2+]i静息水平升高,抑制CaN表达增加,并呈一定的剂量依赖性。结论:黄芪甲苷对苯肾上腺素诱导心肌细胞肥大具有一定的保护作用,其机制可能与抑制细胞内Ca2+进而抑制CaN通路有关。
Objective: To investigate the inhibitory effect of astragaloside Ⅳ on myocardial hypertrophy induced by phenylephrine (PE) and its mechanism. Methods: Cardiomyocyte hypertrophy was induced by 10 μmol / L phenylephrine in vitro. Cyclosporine was treated with different dosages of Astragaloside (12.5, 25 and 50 mg / ml) and calcineurin Inhibition of A (CsA) 1 μmol / L on Phenylephrine - induced Myocardial Hypertrophy. 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 morphological changes of cells were observed by inverted phase contrast microscope. Fura-2 / AM was used as fluorescent probe in Till cation system. [Ca2 +] i transient changes; Werstern blot assay CaN expression. Results Compared with the normal control group, phenylephrine increased the total protein content of cardiomyocytes by 56.2%, the cell volume increased by 79.6%, the resting level of [Ca2 +] i in myocardial cells increased significantly, the expression of CaN increased, (25, 50 mg / ml) can effectively improve phenylephrine-induced cardiomyocyte hypertrophy, inhibit the increase of [Ca2 +] i resting level and inhibit the increase of CaN expression in a dose-dependent manner. CONCLUSION: Astragaloside can protect cardiomyocyte hypertrophy induced by phenylephrine, and its mechanism may be related to inhibition of intracellular Ca2 + and inhibition of CaN pathway.