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Aim:To test the hypothesis that statins inhibit leptin-induced hypertrophy incultured neonatal rat cardiomyocytes.Methods:Cultured neonatal ratcardiomyocytes were used to evaluate the effects of simvastatin on leptin-induced hypertrophy.Intracellular reactive oxygen species(ROS)levels weredetermined by using 2’,7’-dichlorofluorescein diacetate(DCF-DA)fluorescence.Total intracellular RNA and cell protein content,which serve as cell proliferativemarkers,were assayed by using propidium iodide(PI)fluorescence and the Bio-Rad DC protein assay,respectively.The cell surface area,an indicator of cellhypertrophy,was quantified by using Leica image analysis software.Results:After 72 h treatment,leptin markedly increased RNA levels,cell surface area,andtotal cell protein levels in cardiomyocytes,which were significantly inhibited bysimvastatin or catalase treatment.ROS levels were significantly elevated incardiomyocytes treated with leptin for 4 h compared with those cells withoutleptin treatment.The increase in ROS levels in cardiomyocytes induced by leptinwas reversed by treatment with simvastatin and catalase.Conclusion:Simvastatininhibits leptin-induced ROS-mediated hypertrophy in cultured neonatal rat car-diac myocytes.Statin therapy may provide an effective means of improving car-diac dysfunction in obese humans.
Aim: To test the hypothesis that statins inhibit leptin-induced hypertrophy incultured neonatal rat cardiomyocytes. Methods: Cultured neonatal rat cardiomyocytes were used to evaluate the effects of simvastatin on leptin-induced hypertrophy. Intracellular reactive oxygen species (ROS) levels were determined by using 2 ’ , 7’-dichlorofluorescein diacetate (DCF-DA) fluorescence.Total intracellular RNA and cell protein content, which serve as cell proliferative markers, were assayed by using propidium iodide (PI) fluorescence and the Bio-Rad DC protein assay, respectively. surface area, an indicator of cell hypertrophy, was quantified by using Leica image analysis software. Results: After 72 h treatment, leptin markedly increased RNA levels, cell surface area, and total cell protein levels in cardiomyocytes, which were significantly inhibited by simvastatin or catalase treatment. ROS levels were significantly increased in incardiomyocytes treated with leptin for 4 h compared with those cells without leptin treatment . The increase in ROS levels in cardiomyocytes induced by leptinl in turn by treatment with simvastatin and catalase. Confluence: Simvastatin inhibitors of leptin-induced ROS-mediated hypertrophy in cultured neonatal rat car-diac myocytes. Statin therapy may provide an effective means of improving car-diac dysfunction in obese humans.