4.5 Article

Resveratrol, a SIRT1 activator, attenuates aging-associated alterations in skeletal muscle and heart in mice

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JOURNAL OF PHARMACOLOGICAL SCIENCES
卷 152, 期 2, 页码 112-122

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JAPANESE PHARMACOLOGICAL SOC
DOI: 10.1016/jahs.2023.04.001

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Resveratrol; Sarcopenia; Cardiomyocyte hypertrophy; Sirt1; Autophagy

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In this study, the researchers found that resveratrol treatment can alleviate age-related sarcopenia and cardiomyocyte hypertrophy by restoring autophagy. They observed that resveratrol reduces acetylated protein levels and enhances autophagic activity, thus slowing down the aging process.
Aging is associated with impairment of multiple organs, including skeletal muscle and heart. In this study, we investigated whether resveratrol, an activator of an NAD thorn -dependent protein deacetylase Sirtuin-1 (SIRT1), attenuates age-related sarcopenia and cardiomyocyte hypertrophy in mice. Treatment of mice with resveratrol (0.4 g/kg diet) from 28 weeks of age for 32 weeks prevented aging-associated shortening of rotarod riding time. In the tibialis anterior (TA) muscle, histogram analysis showed that the atrophic muscle was increased in 60-week-old (wo) mice compared with 20-wo mice, which was attenuated by resveratrol. In the heart, resveratrol attenuated an aging-associated increase in the cardiomyocyte diameter. Acetylated proteins were increased and autophagic activity was reduced in the TA muscle of 60-wo mice compared with those of 20-wo mice. Resveratrol treatment reduced levels of acetylated proteins and restored autophagic activity in the TA muscle. Aging-related reduction in myocardial autophagy was also suppressed by resveratrol. Skeletal muscle-specific SIRT1 knockout mice showed increases in acetylated proteins and atrophic muscle fibers and reduced autophagic activity in the TA muscle. These results suggest that activation of SIRT1 by treatment with resveratrol suppresses sarcopenia and cardiomyocyte hypertrophy by restoration of autophagy in mice.(c) 2023 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/lice nses/by-nc-nd/4.0/).

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