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Apelin对心肌细胞肥大的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2006年第2期
页码:
185-189
栏目:
基础研究
出版日期:
2006-03-01

文章信息/Info

Title:
Effects of exogenous Apelin on cardiomyocyte hypertrophy
作者:
余洋黄德嘉
四川大学华西医院心血管内科,四川 成都,610041
Author(s):
YU Yang HUANG De-jia
Department of Cardiology,West Hosipital,Sichan University,Chengdu,Sichuan 610041,China
关键词:
Apelin血管紧张素Ⅱ心肌细胞肥大一氧化氮
Keywords:
Apelin angiotensinⅡcardiomyocyte hypertrophy nitric oxide
分类号:
R542.2
DOI:
-
文献标识码:
A
摘要:
目的 近有研究表明在肥大心肌中,“孤儿受体”APJ的内源性配基Apelin减少。由此推测Apelin的水平与心肌细胞肥大可能存在某种联系。本实验旨在观察外源性提高Apelin水平对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的心肌细胞肥大的影响,并探讨其可能的机制。方法 体外培养SpragueDawley乳鼠心肌细胞,进行分组实验。各组在加入干预因素后第5天终止实验。测量心肌细胞的直径、表面积及其蛋白质含量,并测定上清液中一氧化氮(NO)的含量。结果 AngⅡ (0.1 μmol/L)单独作用可引起心肌细胞直径、表面积及蛋白质含量的显著增加(P<0.01),但联合给予Apelin(1 μmol/L)可以减弱AngⅡ诱导的细胞大小及蛋白质含量的增加(P<0.05)。AngⅡ 0.1 μmol/L单独作用时细胞培养液中NO含量显著减少(P<0.01),但联合给予Apelin(1 μmol/L)后细胞培养液中NO含量显著增加(P<0.05)。相关性分析显示培养液中的NO含量分别与以上3种肥大指标呈负相关(r=-0.623,P<0.01;r=-0.731,P<0.01;r=-0.584,P<0.01)。结论 Apelin能够抑制AngⅡ诱导的心肌细胞肥大,这一作用可能与NO生成增加有关。
Abstract:
AIM Recent studies show that in the hypertrophic myocardium, Apelin, the endogenous ligand for the orphan Gproteincoupled receptor APJ, decreases. We then hypothesize that there may exist some relation between Apelin level and cardiac hypertrophy. The purpose of the present study was to examine the effect of exogenous Apelin on angiotensinⅡ(AngⅡ)induced cardiomyocyte hypertrophy and explore the possible underlying mechanism. METHODS Neonatal cardiomyocytes of SD rats were cultured in vitro. Five days after pretreatment, the surface area, the diameter, the protein content of the myocyte and nitric oxide (NO) in the culture solution were measured. RESULTS AngⅡ 0.1 μmol/L alone caused obvious increases in the diameter, surface area and protein content of myocyts(P<0.01),however, coadministration of Apelin(1 μmol/L) inhibited AngⅡinduced increases in cell size and protein content(P<0.05). In addition, AngⅡ 0.1 μmol/Lalone caused a decrease of NO content in the culture solution(P<0.01),but coadministration of Apelin(1 μmol/L) led to increased amount of NO compared with AngⅡ alone(P<0.05). Correlation analysis showed the content of NO in the culture solution had a negative correlation with the above three hypertrophic indexes respectively (r=-0.623, P<0.01; r=-0.731, P<0.01; r=-0.584, P<0.01). CONCLUSION Apelin attenuates angiotensinⅡinduced cardiomyocyte hypertrophy . Nitric oxide seems to play a role in this antihypertropic process.

参考文献/References

[1]Tatemoto K, Hosoya M, Habata Y, et al. Isolation and characterization of a novel endogenous peptide ligand for the human APJ receptor[J]. Biochem Biophys Res Commum, 1998,251(2): 471-476.

[2]Lee DK, Cheng R, Nguyen T, et al. Characterization of Apelin, the ligand for the APJ receptor[J]. J Neurochem, 2000, 74(1): 34-41.

[3]Chen MM, Ashley EA, Deng DX, et al. Novel role for the potent endogenous inotrope Apelin in human cardiac dysfunction[J]. Circulation, 2003,108(12): 1432-1439.

[4]Szokodi I, Tavi P, Foldes G, et al. Apelin, the novel endogenous ligand of the orphan receptor APJ, regulates cardiac contractility[J]. Circ Res, 2002,91(5): 434-440.

[5]Tatemoto K, Takayama K, Zou MX, et al. The novel peptide Apelin lowers blood pressure via a nitric oxidedependent mechanism[J]. Regul Pept, 2001,99(2-3): 87-92.

[6]Foldes G, Horkay F, Szokodi I, et al. Circulating and cardiac levels of Apelin,the novel ligand of the orphan receptor APJ, in patients with heart failure[J]. Biochem Biophys Res Commun, 2003,308(3): 480-485.

[7]Zhan CD,Wang TH,Pan JY. The role of nitric oxide in the angiotensin IIinduced hypertrophy of cardiac myocytes[J] . Sheng Li Xue Bao, 1999,51(6): 660-666.

[8]ScherrerCrosbie M, Ullrich R, Bloch KD, et al. Endothelial nitric oxide synthase limits left ventricular remodeling after myocardial infarction in mice[J]. Circulation,2001,104(11): 1286-1291.

[9]Seki T, Hagiwara H, Naruse K, et al. In situ identification of messenger RNA of endothelial type nitric oxide synthase in rat cardiac myocytes[J]. Biochem Biophys Res Commun, 1996,218(2):601–605.

备注/Memo

备注/Memo:
收稿日期:2004-12-24.作者简介:余洋,医师,硕士 Tel:(028)87394266 Email:fshyang@163.com
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