Abstract
We hypothesized that the phenolic compound resveratrol mitigates muscle protein degradation and loss and improves muscle fiber cross-sectional area (CSA) in gastrocnemius of mice exposed to unloading (7dI). In gastrocnemius of mice (female C57BL/6J, 10 weeks) exposed to a seven-day period of hindlimb immobilization with/without resveratrol treatment, markers of muscle proteolysis (tyrosine release, systemic troponin-I), atrophy signaling pathways, and muscle phenotypic features and function were analyzed. In gastrocnemius of unloaded mice treated with resveratrol, body and muscle weight and function were attenuated, whereas muscle proteolysis (tyrosine release), proteolytic and apoptotic markers, atrophy signaling pathways, and myofiber CSA significantly improved. Resveratrol treatment of mice exposed to a seven-day period of unloading prevented body and muscle weight and limb strength loss, while an improvement in muscle proteolysis, proteolytic markers, atrophy signaling pathways, apoptosis, and muscle fiber CSA was observed in the gastrocnemius muscle. These findings may have potential therapeutic implications in the management of disuse muscle atrophy in clinical settings.
Highlights
Disuse muscle atrophy is relevant in chronic respiratory, cardiac, and kidney diseases, especially in advanced stages
No significant differences were seen in food intake, total body, and gastrocnemius weight between 7 days immobilized (7dI) + Resveratrol mice and the non-treated unloaded mice (Table 1)
Limb strength gain did not further decrease in the immobilized mice treated with resveratrol (Table 1)
Summary
Disuse muscle atrophy is relevant in chronic respiratory, cardiac, and kidney diseases, especially in advanced stages. Conditions such as prolonged immobilization due to bed rest, critical illness, and bone fractures, among others, lead to disuse muscle atrophy in patients [1,2,3]. Several biological mechanisms and pathophysiological alterations take place in the skeletal muscles of patients following disuse muscle atrophy. Those biological events are involved in the process of muscle protein loss, apoptosis, and autophagy. In animal models of disuse muscle atrophy, events such as increased oxidative stress, proteolysis, autophagy, apoptosis, epigenetic modifications, and metabolic derangements have been demonstrated to take place in the muscles exposed to periods of disuse (e.g., immobilization) [9,10,11,12,13,14]
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