作者: Miyuki Kobara , Akiko Furumori-Yukiya , Miho Kitamura , Mihoko Matsumura , Makoto Ohigashi
DOI: 10.1016/J.CARDFAIL.2015.04.016
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摘要: Abstract Background Caloric restriction (CR) prevents senescent changes, in which reactive oxygen species (ROS) have a critical role. Left ventricular (LV) hypertrophy is risk factor for cardiovascular diseases. We examined whether CR alters cardiac redox state and from chronic pressure overload. Methods Results Male c57BL6 mice were subjected to ascending aortic constriction (AAC) with ad libitum caloric intake (AL + AAC group) or 40% restricted (CR + group). was initiated 2 weeks before continued 4 weeks. Two after constriction, increased LV wall thickness, impaired transmitral flow velocity, augmented myocyte fibrosis, association enhancement of BNP collagen III expressions the AL + group. In group, oxidative stress tissue mitochondria enhanced, NADPH oxidase activity mitochondrial ROS production elevated. These changes significantly attenuated CR + Additionally, antioxidant systems, myocardial glutathione peroxidase superoxide dismutase activities enhanced Conclusions Chronic overload damage, fibrosis. Short-term suppressed improved function, suggesting that short-term could be useful strategy prevent overload–induced injury.