我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

TNF-α对培养乳鼠心肌细胞的作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2012年第3期
页码:
331-334
栏目:
基础研究
出版日期:
2012-06-25

文章信息/Info

Title:
Effect of TNF-α on cultured neonate cardiomyocytes
作者:
苏兴利1; 张 鸿2; 王 爽1; 郭玉芳1; 霍 健1; 杨 颖3; 杨予白4
(西安医学院:1.基础医学部病理生理学教研室，3.科研中心，陕西 西安 710021；2.陕西省人民 医院传染科，陕西 西安 710068；4.西安交通大学医学院病理生理教研室，陕西 西安 710061)
Author(s):
SU Xing-li1;  ZHANG Hong2;  WANG Shuang1;  GUO Yu-fang1;  HUO Jian1;  YANG Ying3;  YANG Yu-bai4
(1.Department of Pathophysiology, 3.Scientific Research Centre, Xi’an Medical University, Xi’an 710021, Shaanxi, China; 2.Department Of Infectious Diseases, Shaanxi Provincial People’s Hospital, Xi’an 710068, Shaanxi, China; 4.Department of Pathophysiology, Xi’an Jiaotong University, Xi’an 710061, China)
关键词:
心肌细胞; 肿瘤坏死因子α; 血管紧张素Ⅱ; AT1受体; 心肌改建; 乳鼠
Keywords:
TNF-α;  AngII;  AT1 receptor;  cardiac remodeling;  cardiomyocyte
分类号:
R392.12
DOI:
-
文献标识码:
A
摘要:
目的:探讨不同浓度肿瘤坏死因子-α(TNF-α)对培养的乳鼠心肌细胞活力、蛋白合成、分泌AngⅡ及AT1受体表达的影响。方法： 体外培养的SD乳鼠心肌细胞随机分为对照组和不同浓度TNF-α（20、40、60、80、100 μg/L）干预组，用BCA法测定心肌细胞蛋白合成总量，MTT比色法和LDH检测反映心肌细胞的活力，ELISA法检测心肌细胞培养液中AngⅡ的含量，免疫细胞化学染色法检测心肌细胞膜AT1受体表达的变化。结果： TNF-α浓度依赖性地增强乳鼠心肌细胞活力、增加蛋白合成，20、40、60、80 μg/L TNF-α组细胞活力较对照组分别增加1.21（P<0.05)、1.42、1.51和1.73倍（均P<0.01)，蛋白合成分别增加27.8%（P<0.05）、38.9%、46%和66.7%（均P<0.01），而LDH含量差异无显著性。100 μg/L TNF-α组与对照组比较，心肌细胞活力降低18.5%（P<0.01）、蛋白合成降低18.3%（P<0.01）及心肌LDH生成增加1.48倍（P<0.01)。TNF-α浓度依赖性地增加乳鼠心肌细胞AngⅡ分泌，与对照组比较分别增加0.5、1.1、1.6、3和3.6倍（均P<0.01）。TNF-α还具有诱导AT1受体的表达的作用。结论： TNF-α可促进心肌细胞内源性AngⅡ产生，引起心肌细胞活力、蛋白合成改变，AT1受体表达上调，可能介导了心肌肥大、心肌受损等心肌改建的病理生理过程。
Abstract:
AIM:To explore the effects of TNF-α of different concentrations on cardiomyocyte vitality, protein synthesis, AngII secretion and AT1 receptor expression. METHODS: Cardiomyocytes were primarily cultured in Sprague Dawley neonate rats. Protein and cell vitality of myocytes were determined, respectively, by BCA method and MTT and LDH assay. Content of AngII in cell culture fluid was detected by enzyme-linked immunosorbent assay and expression alteration of AT1 receptor in myocytes was examined by immunocytochemical assay. RESULTS: TNF-α promoted AngII secretion in cardiomyocytes in a concentration-dependent manner. Low concentrations of TNF-α increased cell viability and promoted protein synthesis and AT1 receptor expression in myocytes. High concentrations of TNF-α induced myocyte injury. CONCLUSION: TNF-α promotes the secretion of AngII in myocytes and is involved in cardiac remodeling.

参考文献/References

[1]Lin L,Gong H,Ge J,et al.High density lipoprotein downregulates angiotensin II type 1 receptor and inhibits angiotensin II-induced cardiac hypertrophy[J].Biochem Biophys Res Commun,2011,404(1):28-33.

[2]Sriramula S,Haque M,Majid DS,et al.Involvement of tumor necrosis factor-alpha in angiotensin II-mediated effects on salt appetite, hypertension, and cardiac hypertrophy[J].Hypertension,2008,51(5):1345-1351.

[3]Kalra D,Sivasubramanian N,Mann DL.Angiotensin II induces tumor necrosis factor biosynthesis in the adult mammalian heart through a protein kinase C-dependent pathway[J].Circulation,2002,105(18):2198-2205.

[4]Yokoyama T, Sekiguchi K,Tanaka T,et al.Angiotensin II and mechanical stretch induce production of tumor necrosis factor in cardiac fibroblasts[J].Am J Physiol,1999,276 (6 Pt 2):H1968-H1976.

[5]Haudek SB,Taffet GE,Schenider MD,et al.TNF provokes cardiomyocyte apoptosis and cardiac remodeling through activation of multiple cell death pathways[J].J Clin Invest,2007,117(9):2692-2701.

[6]von Haehling S,Jankowska EA,Anker SD.Tumour necrosis factor-alpha and the failing eart-pathophysiology and therapeutic implications[J].Basic Res Cardiol,2004,99(1):18-28.

[7]苏兴利,高广道,罗秀成,等.大鼠压力负荷性肥大心肌中TNF-α mRNA表达变化[J].中国病理生理杂志,2004,20(8):1414-1417.

[8]Allen AM, Zhuo J, Mendelsohn FA. Localization and function of angiotensin AT1 receptors[J].Am J Hypertens,2000,13(1 Pt 2):31S-38S.

[9]Mehta PK,Grindling KK.Angiotensin cell signaling:physiological and pathological effects in the cardiovascular system[J].Am J Physiol Cell Physiol,2007,292(1):C82-C97.

[10]Arenas IA,Xu Y,Lopez-Jaramillo P,Davidge ST. Angiotensin II-induced MMP-2 release from endothelial cells is mediated by TNFalpha[J].Am J Physiol Cell Physiol,2004,286(4):C779-C784.

[11]Dai W,Chen H,Jiang J,et al.Silencing MR-1 attenuates inflammatory damage in mice heart induced by AngII[J].Biochem Biophys Res Commun,2010,391(3):1573-1578.

[12]Zera T,Ufnal M,Szczepanska-Sadowska E.Central TNF-alpha elevates blood pressure and sensitizes to central pressor action of angiotensin II in the infarcted rats[J].J Physiol Pharmacol,2008,59(Suppl 8):117-121.

备注/Memo

备注/Memo:
收稿日期：2011-07-24.基金项目：陕西省卫生厅科学研究基金项目资助（06D15），陕西省教育厅自然科学研究计划项目资助（08JK421） 通讯作者：苏兴利，副教授，主要从事心血管病理生理学的研究 Email:suxingli@126.com
更新日期/Last Update: 2012-05-02