盐负荷和醛固酮诱导乳鼠原代心肌细胞肥大的实验研究

Abstract
Figure/Table
References (20)
Related Citation (4)

Download: PDF (894 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To investigate the synergistic effects of salt loading and aldosterone on hypertrophy of primary cardiomyocytes in neonatal rats. Methods Neonatal rat cardiomyocytes were culturedin the experiment, the cell was divided into normal control group, Aldosterone 10-7 mol/L (Ald) group, normal sodium concentration 140 mmol/L (NS) group, high sodium concentration 146 mmol/L (HS) group, 140 mmol/L+Ald 10-7 mol/L (NS+Ald) group, 146 mmol/L+Ald 10-7mol/L (HS+Ald) group. At first Ald was not added into (NS+Ald) group and (HS+Ald) group, after 48 h culture, Ald was added, then all treatment groups were continued to culture for 24 h. The difference of myocardial cross-sectional area was measured by immunofluorescence. The survival rate was detected by CCK-8. The apoptosis rate was detected by flow cytometry. ET-1 and eNOS mRNA expressions were assayed by qRT-PCR. Results The cross-sectional area of myocardial cells in NS+Ald group and HS+Ald group were significantly higher than Ald group, NS group, HS group. Compared with normal control group, the survival rate of cardiomyocytes decreased significantly (P < 0.01) and apoptosis rate increased significantly (P < 0.01) in NS+Ald group and HS+Ald group; except for NS group, ET-1 mRNA expression increased and eNOS mRNA expression decreased in other groups, the effect of HS+Ald group was the most significant (P < 0.01). Conclusion Salt loading and aldosterone are important participation factors which induced cardiomyocyte hypertrophy, they have synergistic effects. Among them, aldosterone-induced cardiomyocyte hypertrophy is the most significant in high salt condition.

Key words： Salt load Aldosterone Myocardial cell Gene expression Apoptosis

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	YOU Shuping1 JIANG Hong1 HE Lijuan2 TAO Ning2 WANG Zhong2 CHEN Qingjie3 LIU Tao2

Cite this article:

YOU Shuping1 JIANG Hong1 HE Lijuan2 TAO Ning2 WANG Zhong2 CHEN Qingjie3 LIU Tao2. Experimental research on effect of hypertrophy of primary cardiomyocytes in suckling mouse induced by salt loading and aldosterone[J]. 中国医药导报, 2017, 14(28): 13-16.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2017/V14/I28/13

[1] 由淑萍，从美丽，倪国华，等.哈萨克族原发性高血压病患者全血DNA甲基化位点筛查及异常甲基化谱的构建[J].中国全科医学，2017，20（6）：678-683.
[2] 由淑萍，詹怀峰，王红军，等.新疆南山牧区哈萨克族人群高血压患病率及危险因素分析[J].现代预防医学，2017， 44（5）：863-866，902.
[3] 高斐.高盐摄入加速诱导的高血压性左室重塑及心脏淋巴管变化的实验研究[D].天津：天津医科大学，2011：10-15.
[4] Mimran A，Du Cmlar G. Dietary sodium：the dark horse amongst cardiovascular and renal risk factors [J]. Nephrol Dial Transplant，2008，23（7）：2138-2141.
[5] Liu HB，Zhang J，Sun YY，et al. Dietary salt regulates epithelial sodium channels in rat endothelial cells：adaptation of vasculature to salt [J]. Br J Pharmacol，2015，172（23）：5634-5646.
[6] 陶静，马依彤，李晓梅，等.原代乳鼠心肌细胞培养方法的改进[J].中华心血管病杂志，2014，42（1）：53-56.
[7] 由淑萍，赵军，马龙，等.肉苁蓉苯乙醇总苷及其单体对肝星状细胞增殖和凋亡的影响[J].癌变·畸变·突变，2017， 29（1）：13-17，22.
[8] 赵勤，杨进.醛固酮参与左心室重构研究新进展[J].世界临床医学，2017，11（12）：117-118.
[9] Vinod P，Krishnappa V，Chauvin AM，et al.Cardiorenal syndrome：role of arginine vasopressin and vaptans in heart failure [J]. Cardiol Res，2017，8（3）：87-95.
[10] Feola M，Monteverde M，Vivenza D，et al. Prognostic value of different allelic polymorphism of aldosterone synthase receptor in a congestive heart failure european continental ancestry population [J]. Arch Med Res，2017，48（2）：156-161.
[11] Wagner M，Rudakova E，Volk T. Aldosterone-induced changes in the cardiac L-type Ca2+ current can be prevented by antioxidants in vitro and are absent in rats on low salt diet [J]. Pflugers Arch，2008，457（2）：339-349.
[12] 吉村道博.醛固酮和食盐促进心肌肥大的机制——MR阻断剂的作用点[J].日本医学介绍，2007，28（5）：208-211.
[13] 王桂君，姚玉胜，王洪新.肿瘤坏死因子α通过PI3K-IP3R-Ca2+途径诱导乳鼠心肌肥大[J].中国病理生理杂志，2016，32（1）：21-26.
[14] 黄世亮，郭瑞威，匡陈伟，等.钠钙交换体1在高血压发病学中的研究进展[J].西南国防医药，2016，26（2）：215-217.
[15] Frustaci A，Chimenti C，Setoguchi M，et al. Cell death in acromegalic cardiomyopathy[J].Circulation，1999，99：1426-1434.
[16] Mizuno Y，Yasue H，Yoshimura M，et al. Effects of perindopril on aldosterone production in the failing human heart [J]. Am J Cardiol，2002，89（10）：1197-1200.
[17] Balakumar P，Kathuria S，Taneja G，et al. Is targeting eNOS akey mechanistic insight of cardiovascular defensive potentials of statins [J]. J Mol Cell Cardiol，2012，52（1）：83-92.
[18] Liu Y，Feng Q. NOing the heart：role of nitric oxide synthase-3 in heart development [J]. Differentiation，2012， 84（1）：54-61.
[19] 黄小阳，李卓明，刘志平，等.SIRT6通过调节eNOS抑制心肌肥大的机制研究[J].中山大学学报：医学科学版，2015，36（3）：338-345.
[20] 孔令雷，颜玲娣，宫泽辉.内皮素系统与心肌肥厚[J].中国药理学通报，2008，24（9）：1127-1130.