Abstract
Transverse aortic constriction (TAC)-induced pressure overload (PO) causes adverse cardiac remodeling and dysfunction that progresses to heart failure (HF). The purpose of this study was to determine whether the potent antioxidant, resveratrol, significantly attenuates PO-induced HF in wild-type mice. Male C57BL6 mice were subjected to either sham or TAC surgery. One group of TAC mice was given daily resveratrol treatment. Echocardiographic, biometric, and immunohistological analyses were performed on the three groups of mice. All echocardiographic parameters demonstrated significantly greater adverse cardiac remodeling and dysfunction in the TAC compared to the sham mice. Increases in the ratios of heart weight (HW)/body weight (BW) and lung weight (LW)/BW and a sharp decline in the percentage of ejection fraction and fractional shortening were found in TAC relative to sham mice. Likewise, the TAC protocol increased markers of oxidative stress, cardiac hypertrophy, inflammation, fibrosis, hypoxia, and apoptosis. These pathological changes were significantly attenuated by resveratrol treatment. Resveratrol treatment significantly attenuates the adverse cardiac remodeling and dysfunction produced by the TAC protocol in C57/BL6 mice and this activity is mediated, at least in part, by the inhibition of oxidative stress and inflammation indicating a therapeutic potential of resveratrol in HF.
Highlights
Heart failure (HF) is a primary cause of morbidity and mortality in many parts of the world. (Wu et al 2002; Liew and Dzau 2004)
Analysis of mice after 4 weeks of pressure overload (PO) showed that heart weight (HW) to body weight (BW) ratios were significantly greater in Transverse aortic constriction (TAC) mice compared to sham-operated mice (Fig. 1A)
The ratio of lung weight (LW) to BW was significantly higher in TAC mice compared to sham mice (Fig. 1B) The increases in HW/BW and LW/BW ratios after TAC were significantly attenuated by resveratrol treatment (Fig. 1A and B)
Summary
Heart failure (HF) is a primary cause of morbidity and mortality in many parts of the world. (Wu et al 2002; Liew and Dzau 2004). Cardiac hypertrophy is an adaptation that is beneficial to the stressed heart in the initial stages wherein cardiomyocytes enlarge in size to achieve adequate function in the presence of chronic pathological stress (Frey and Olson 2003) this compensatory phase is temporary because in the face of continued stress the heart eventually enters into a decompensatory stage (Adler et al 2011). This transition from compensatory to decompensatory stage is characterized by marked increases in cardiac fibrosis, hypoxia, and apoptosis that lead to irreversible functional changes and HF (Juric et al 2007; Wojciechowski et al 2010; Yu and Li 2010).
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