肿瘤坏死因子-α诱导心肌肥大中CaN信号通路的作用

目的:研究钙调神经磷酸酶(CaN)信号通路在肿瘤坏死因子-α(TNF-α)诱导心肌细胞肥大中的作用。方法:Lowry法测心肌细胞蛋白含量;计算机图象分析系统测心肌细胞体积;[3H]-亮氨酸掺入法测心肌细胞蛋白合成;Till阳离子测定系统观察胞内[Ca2+]i瞬变;Western blot法测定CaN的表达。结果:①CaN特异性抑制剂CsA(0.2μmol/L)明显抑制TNF-α(100μg/L)诱导的心肌细胞蛋白含量、蛋白合成和细胞体积增大,但对正常心肌细胞生长无影响。②CaN特异性抑制剂CsA(0.2μmol/L)明显降低TNF-α诱导的心肌细胞内钙离子浓度([Ca2+]i)瞬变幅度增高。③TNF-α明显增强心肌细胞内CaN的表达。结论:TNF-α可能通过引起心肌细胞[Ca2+]i升高,促进CaN表达诱导心肌细胞肥大。

Calcineurin contributed to tumor necrosis factor alpha-induced cardiomyocyte hypertrophy in rats

Objective: To investigate whether calcineurin(CaN) contribute to tumor necrosis factor α(TNF-α)-induced cardiomyocyte hypertrophy.Methods: The protein content was assayed with lowry’s method.The cardiomyocytes volumes were measured by computer photograph analysis system.The protein synthesis was assayed with -leucine incorporation method.i transient was measured by Till image system by cell-loading Fura-2/AM.The expression of CaN was determined by Western blot.Results: ①CsA(0.2 μmol/L),a selective CaN inhibitor,significantly suppressed the increase of protein content,-leucine incorporation and cell size induced by TNF-α.②CsA(0.2 μmol/L)significantly suppressed the elevation of the amplitude of the spontaneous Ca2+ transients induced by TNFα in cultured ventricular myocytes from the neonatal rat.③TNF-α significantly increased the expression of CaN.Conclusion: Ca2+-CaN signaling pathway are involved in cardiomyocyte hypertrophy induced by TNF-α in rats.