Document Type: Original paper
Department of Physiology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Yazd Cardiovascular Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Department of Biochemistry, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
School of Veterinary Medicine, Shiraz University, Shiraz, Iran.
Department of Physiology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.Biotechnology Research Center, International Campus, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Background and objectives: Resveratrol(3,5,4′-trihydroxy-trans-stilbene) is a natural polyphenole phytoalexin which exerts potential cardioprotective effects, but the cellular and molecular mechanisms responsible for these effects are still unknown. Cardiac renin angiotensin system (RAS) over-activation plays an important role in pathogenesis of left ventricular hypertrophy (LVH) progression. The aim of the study was to investigate the effects of resveratrol on the main components of RAS during early and late phase of myocardial hypertrophy. Methods: To consider the early and late phase of LVH, the rats were studied two and sixteen weeks after abdominal aorta banding without treatment (H2w and H16w groups, respectively) or with resveratrol (R) treatment. Intact animals served as control (Ctl). Arterial blood pressure was recorded by carotid cannulation. Angiotensin II (Ang II) level was measured using ELISA kit. Gene expression was evaluated by Real time RT-PCR technique. Cardiomyocyte size and fibrosis were assessed using haematoxylin/eosin and Masson trichrome staining, respectively Results: Results of this study showed that in H2w group AT1a mRNA level was increased significantly (pConclusion: Progression of LVH is accompanied by dynamic changes in RAS components expression in myocardial tissue. Resveratrol protects the heart against pressure overload-induced hypertrophy in part via RAS suppression.