肿瘤坏死因子-α诱导心肌肥大中CaN信号通路的作用  

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

作　　者：王桂君[1] 姚玉胜[2] 王洪新[3] 郭莲怡[1] 

机构地区：[1]辽宁医学院附属第一医院,锦州121000 [2]辽宁医学院附属第二医院,锦州121000 [3]辽宁医学院药理学教研室,锦州121000

出　　处：《中国应用生理学杂志》2012年第2期184-188,共5页Chinese Journal of Applied Physiology

基　　金：辽宁省教育厅一般项目(L2010304;2009A455);辽宁省科技厅项目(2010225034)

摘　　要：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。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.

关 键 词：心肌肥大 肿瘤坏死因子-Α 钙离子 钙调神经磷酸酶 

分 类 号：R972[医药卫生—药品]