Chinese Medical Sciences Journal ›› 2015, Vol. 30 ›› Issue (4): 245-251.doi: 10.1016/S1001-9294(16)30008-6

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Effect of Atorvastatin on Expression of Peroxisome Proliferator-activated Receptor Beta/delta in Angiotensin Ⅱ-induced Hypertrophic Myocardial Cells In Vitro

Li Sheng1, Xu Yang1, Ping Ye1, Yong-xue Liu2, Chun-guang Han2   

  1. 1.Department of Geriatric Cardiology, Chinese PLA General Hospital, Beijing 100853, China;
    2.Department of Pharmacology & Toxicology, Beijing Institute of Radiation Medicine, Beijing 100850, China
  • Received:2015-04-07 Published:2015-12-20 Online:2015-12-20

Objective To explore the effect of atorvastatin on cardiac hypertrophy and to determine the potential mechanism involved.Methods An in vitro cardiomyocyte hypertrophy from neonatal rats was induced with angiotensinⅡ (Ang Ⅱ) stimulation. Before AngⅡ stimulation, the cultured rat cardiac myocytes were pretreated with atorvastatin at different concentrations (0.1, 1, and 10 μmol/L). The following parameters were evaluated: the myocyte surface area, 3H-leucine incorporation into myocytes, mRNA expressions of atrial natriuretic peptide, brain natriuretic peptide, matrix metalloproteinase 9, matrix metalloproteinase 2, and interleukin-1β, mRNA and protein expressions of the δ/β peroxisome proliferator-activated receptor (PPAR) subtypes.Results It was shown that atorvastatin could ameliorate Ang Ⅱ-induced neonatal cardiomyocyte hypertrophy in the area of cardiomyocytes, 3H-leucine incorporation, and the expression of atrial natriuretic peptide and brain natriuretic peptide markedly. Meanwhile, atorvastatin also inhibited the augmented mRNA level of several cytokines in hypertrophic myocytes. Furthermore, the down-regulated expression of PPAR- δ/β at both the mRNA and protein levels in hypertrophic myocytes could be significantly reversed by atorvastatin treatment.Conclusions Atorvastatin could improve AngⅡ-induced cardiac hypertrophy and inhibit the expression of cytokines. Such effect might be partly achieved through activation of the PPAR-δ/β pathway.

Key words: peroxisome proliferator-activated receptor, cardiac hypertrophy, statin, angiotensinⅡ

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