Iranian journal of basic medical sciences · 2026
Role of gallic acid in sarcopenia in D-galactose-treated mice.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Ошибки и ограничения
История · было → стало
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Liu Xianchu, Zhu Zile, Liu Ming, Mao Zhihe
Аннотация
OBJECTIVES: Aging is a natural phenomenon that results in sarcopenia to impair living quality in humans. Gallic Acid (GA) has many biological activities against aging and muscle injury. Our purpose was to clarify possible mechanisms of GA on aged-relevant sarcopenia.
MATERIALS AND METHODS: Senescent model was established by D-galactose in mice. The senescent model was treated with GA for 10 weeks. Skeletal muscle was stained via HE to assess muscle fiber size. Oxidation indicators and inflammatory factors were detected using a spectrophotometer and ELISA. The protein expressions were tested by Western blot.
RESULTS: Our data unveiled GA enhanced muscle mass to improve grip strength and fatigue in D-galactose-induced aging mice. In serum, GA increased T-AOC, SOD and CAT levels, and decreased MDA, TNF-α, and IL-6 levels to exert its anti-oxidative and anti-inflammatory properties. In skeletal muscle, GA decreased atrogin 1, Murf-1, collagen I, and Tgf-β1 expressions to improve atrophy and fibrosis. Furthermore, GA increased Pgc-1α, Nrf-1, Beclin-1, and Bcl-2 expressions, and decreased P62 and Bax expressions to prevent skeletal muscle damage.
CONCLUSION: GA exerted its protective effects on sarcopenia concomitant aging via moderating mitochondrial biology, enhancing autophagy and restraining apoptosis.
MATERIALS AND METHODS: Senescent model was established by D-galactose in mice. The senescent model was treated with GA for 10 weeks. Skeletal muscle was stained via HE to assess muscle fiber size. Oxidation indicators and inflammatory factors were detected using a spectrophotometer and ELISA. The protein expressions were tested by Western blot.
RESULTS: Our data unveiled GA enhanced muscle mass to improve grip strength and fatigue in D-galactose-induced aging mice. In serum, GA increased T-AOC, SOD and CAT levels, and decreased MDA, TNF-α, and IL-6 levels to exert its anti-oxidative and anti-inflammatory properties. In skeletal muscle, GA decreased atrogin 1, Murf-1, collagen I, and Tgf-β1 expressions to improve atrophy and fibrosis. Furthermore, GA increased Pgc-1α, Nrf-1, Beclin-1, and Bcl-2 expressions, and decreased P62 and Bax expressions to prevent skeletal muscle damage.
CONCLUSION: GA exerted its protective effects on sarcopenia concomitant aging via moderating mitochondrial biology, enhancing autophagy and restraining apoptosis.