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

Objective To explore the effect of atorvastatinpotential mechanism involved.on cardiac hypertrophy and to determine the Methods An in vitro cardiomyocyte hypertrophy from neonatal rats was induced with angiotensinII（Ang Ⅱ） stimulation. Before Ang Ⅱ stimulation, the cultured rat cardiac myocytes were pretreated withatorvastatin 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 natriureticpeptide, brain natriuretic peptide, matrix metalloproteinase 9, matrix metalloproteinase 2, and interleukin-1~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 cardiomyocytehypertrophy in the area of cardiomyocytes, 3H-leucine incorporation, and the expression of atrial natriureticpeptide and brain natriuretic peptide markedly. Meanwhile, atorvastatin also inhibited the augmented mRNAlevel 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 byatorvastatin treatment. Conclusions Atorvastatin could improve Ang Ⅱ-induced cardiac hypertrophy and inhibit theexpression of cytokines. Such effect might be partly achieved through activation of the PPAR-δ/β pathway.