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中国临床药理学与治疗学 ›› 2013, Vol. 18 ›› Issue (7): 721-724.

• 基础研究 •    下一篇

不同剂量前列腺素E2对H9c2心肌细胞肥大的影响

戴珩1, 左中2, 陈萍1, 高进1, 熊秋菊1   

  1. 1重庆医科大学附属第一医院麻醉科;
    2心内科,重庆 400016
  • 收稿日期:2012-08-10 修回日期:2012-11-19 出版日期:2013-07-26 发布日期:2013-06-20
  • 通讯作者: 陈萍,女,教授,硕导,研究方向:麻醉与重要脏器保护。Tel: 023-89011069 E-mail: mazuichen@163.com
  • 作者简介:戴珩,女,在读硕士,研究方向:麻醉与重要脏器保护。Tel: 15823826847 E-mail: daiheng77@gmail.com
  • 基金资助:
    卫生部国家临床重点专科[财社〔2011〕170];重庆市医学重点学科[渝卫科教〔2007〕2号];重庆市卫生局医学科研重点项目(2012-1-018)

Influence of prostaglandin E2 on hypertrophy in H9c2 cardiac cells

DAI Heng1, ZUO Zhong2, CHEN Ping1, GAO Jin1, XIONG Qiu-ju1   

  1. 1Department of Anesthesiology;
    2Department of Cardiology, the First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China
  • Received:2012-08-10 Revised:2012-11-19 Online:2013-07-26 Published:2013-06-20

摘要: 目的: 研究前列腺素E2(PGE2)对H9c2心肌细胞的肥大作用,并分析其量效关系,为寻找抗心肌肥大的潜在靶点提供理论依据。方法: 将H9c2心肌细胞分为空白对照组(C组)和PGE2处理组,PGE2处理组又分为小剂量PGE2组(D1组)、中剂量PGE2组(D2组)和大剂量PGE2组(D3组)。各组细胞培养液中PGE2终浓度分别为0、0.1、1及 10 μmol/L。给药孵育 48 h 后,利用荧光显微镜观察大鼠H9c2心肌细胞形态及体积;通过测量细胞直径大小、BCA法测定细胞总蛋白含量来确定心肌细胞是否肥大;RT-PCR技术测量心钠肽(Atrial natriuretic peptide, ANP)、脑钠肽(Brain natriuretic peptide, BNP) mRNA的表达水平,以此判断是否发生病理性肥大。结果: 与C组比较,免疫荧光显示D1组、D2组及D3组细胞形态改变、体积增大;细胞直径及总蛋白含量显著增加(P<0.05),不同剂量PGE2组间亦具有统计学差异(P<0.05);D2组及D3组较C组细胞内ANP、BNP mRNA表达水平显著增高(P<0.05)。结论: PGE2可剂量依赖地诱导H9c2心肌细胞肥大,较大剂量PGE2引发心肌细胞病理性肥大。抑制PGE2合成有望为抑制心肌肥大提供靶点。

关键词: 前列腺素E2, 环氧化酶, 心肌细胞, 细胞肥大

Abstract: AIM: To explore the effects of PGE2 on cardiomyocyte through experiments on the cultured H9c2 cardiac cells, assess the dose-effect relationship to provide the basic theory for looking for potential targets of inhibiting myocardial hypertrophy.METHODS: H9c2 cardiac cells were randomly divided into four groups: control group (group C), 0.1 μmol/L PGE2 group (group D1), 1 μmol/L PGE2 group (group D2) and 10 μmol/L PGE2 group (group D3). Forty-eight hours later after PGE2 was fed, the morphology of H9c2 cardiac cells were recorded by using a fluorescence microscope. The occurrence of myocardial hypertrophy was observed in terms of cell diameter and total protein of the cells. And the gene expression levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) mRNA in cells, which were measured by RT-PCR, helped to judge whether there was an occurrence of pathological myocardial hypertrophy.RESULTS: Compared with group C, the cell shape changed and the volume increased, the cell diameter and the total protein were increased in group D1, group D2 and group D3 (P<0.05). There were also significant differences between different doses of PGE2 (P<0.05); the expression levels of ANP and BNP mRNA were upregulated in group D2 and group D3 compared with group C (P<0.05).CONCLUSION: PGE2 can induce myocardial hypertrophy of the cultured H9c2 cardiac cells in a dose-dependent manner. Larger dose of PGE2 stimulate pathological myocardial hypertrophy. Inhibition of PGE2 is expected to be a new target to control myocardial hypertrophy.

Key words: Prostaglandin E2, Cycloxygenase, Myocardial hypertrophy

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