Key result
Atorvastatin ameliorated Ang II-induced neonatal cardiomyocyte hypertrophy and inhibited cytokine expression, partly through activation of the PPAR-δ/β pathway.
Atorvastatin attenuates angiotensin II-induced cardiomyocyte hypertrophy in vitro, potentially through the activation of the PPAR-δ/β pathway.
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May inform mechanistic research on atorvastatin in hypertrophy; leaves open in vivo and clinical translation.
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 angiotensin II (Ang II) stimulation. Before Ang II 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 Ang II-induced cardiac hypertrophy and inhibit the expression of cytokines. Such effect might be partly achieved through activation of the PPAR-δ/β pathway.
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Sheng et al. (2015) studied Cardiac hypertrophy. Atorvastatin vs. Angiotensin II stimulation alone was evaluated on Cardiomyocyte hypertrophy (myocyte surface area, 3H-leucine incorporation, and expression of ANP and BNP). Atorvastatin ameliorated Ang II-induced neonatal cardiomyocyte hypertrophy and inhibited cytokine expression, partly through activation of the PPAR-δ/β pathway.
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