钙离子在肿瘤坏死因子α诱导心肌肥大中的作用  

The Role of Calcium in Cardiomyocyte Hypertrophy Induced by Tumor Necrosis Factor-α

作　　者：王桂君[1] 郭莲怡[1] 王洪新[2] 

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

出　　处：《中国动脉硬化杂志》2013年第1期47-51,共5页Chinese Journal of Arteriosclerosis

基　　金：辽宁省教育厅项目(L2010304;2009A455);辽宁省科技厅计划项目(2010225034)

摘　　要：目的研究Ca2+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;计算机图像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。结果 IP3R阻断剂2-APB(30μmol/L)或RyR阻断剂ryanodine(50μmol/L)能降低由TNF-α(100μg/L)诱导的心肌细胞蛋白合成、蛋白含量以及细胞体积增加,二者合用抑制作用更强。L型Ca2+通道阻断剂nifedipine(50μmol)对上述反应无明显作用(P>0.05)。IP3R阻断剂2-APB(30μmol/L)或RyR阻断剂ryanod-ine(50μmol/L)能降低由TNF-α(100μg/L)诱导的心肌细胞内钙离子瞬变幅度增高,二者合用作用抑制更强。L型Ca2+通道阻断剂nifedipine(50μmol/L)对其无明显作用(P>0.05)。结论 TNF-α通过调节心肌细胞内钙离子浓度从而诱导心肌细胞肥大。而在此过程中TNF-α可能主要是通过作用IP3R和RyR促使胞内钙贮库Ca2+释放而引起胞内钙离子水平增高的,而非通过打开L型Ca2+通道。Aim To investigate the role of calcium in tumor necrosis factor ct （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 [ 3H ]-leucine incorporation method. [ Ca2 ＋ ] i transient was measured by Till image system by cell-loading Fura-2/AM. Results 2-APB, a selective IP3 R inhibitor, and/or ryanodine, a selective RyR inhibitor, significantly suppress the elevation of the amplitude and the rates of the spontaneous Ca2＋ transients induced by TNF-α in cultured ventricular myocytes from the neonatal rat. Nifedipine, an L-type calcium channels antagonist, had little effect on it. The increase of protein content, 3 H-leucine incorporation and cell size induced by TNF-α were significantly suppressed by 2-APB, and/or ryanodine. Nifedipine had no effect on it. Conclusion TNF-α induced cardiac hypertrophy through increasing of intracellular Ca2＋ in cultured ventricular myocytes from the neonatal rat. It was induced by both IP3 R and RyR, not by L-type calcium channels.

关 键 词：心肌肥大 肿瘤坏死因子Α 钙离子 IP3R RYR 

分 类 号：R972[医药卫生—药品]