Journal of ethnopharmacology · 2026
A standardized Eleutherococcus senticosus stem extract attenuates dexamethasone-induced skeletal muscle atrophy.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Lee Jueon, Shin Sujin, Park Junkyu, Kim Youngmin, Choi Ho-Young, Bu Youngmin, Cho Ju-Hyun, Choi Ye-Eun, Lee Kyungjin
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Eleutherococcus senticosus (Rupr. & Maxim.) Maxim. is a well-established traditional adaptogen traditionally used to strengthen muscles and bones, suggesting potential relevance in muscle wasting conditions. However, its stems remain underutilized compared with the roots. As a sustainable aerial resource, the stem represents a practical target for standardized ethnopharmacological development. Therefore, this study aimed to evaluate the anti-atrophic efficacy of a standardized E. senticosus stem water extract (ES-SW) against dexamethasone (DEX)-induced skeletal muscle atrophy.
MATERIALS AND METHODS: Male Sprague-Dawley rats received ES-SW (100 and 300 mg/kg, p. o.) for 3 weeks, with DEX (0.5 mg/kg, i. p.) co-administered during the final 2 weeks. Muscle function, muscle mass, and tibialis anterior histomorphometry were assessed. Serum insulin-like growth factor-1 (IGF-1), creatine kinase-MM (CK-MM), and plasma interleukin-6 (IL-6) levels were quantified. In C2C12 myotubes, the effects of ES-SW on DEX-induced (50 μM) atrophy and proteostasis-related signaling pathways were evaluated.
RESULTS: DEX treatment induced a catabolic phenotype characterized by reduced grip strength, muscle mass, and myofiber cross-sectional area, along with decreased IGF-1 and increased CK-MM and IL-6 levels. ES-SW dose-dependently attenuated these functional and structural deteriorations, with the 300 mg/kg group exhibiting the most pronounced protective effects. In skeletal muscle, ES-SW increased the phosphorylation of FoxO3a and suppressed the expression of the atrogenes, muscle atrophy F-box and muscle RING finger-1, and modulated autophagy-associated protein turnover, as reflected by changes in LC3B and p62 expression. In C2C12 myotubes, ES-SW mitigated DEX-induced myotube atrophy and was associated with modulation of FoxO3a and Akt/mTOR signaling.
CONCLUSIONS: Standardized ES-SW effectively attenuated DEX-induced muscle atrophy, accompanied by suppression of FoxO3a-associated atrogene expression, with supportive in vitro evidence suggesting involvement of regulatory pathways associated with muscle protein turnover. These findings support ES-SW as a sustainable ethnopharmacological candidate for the management of glucocorticoid-associated muscle wasting.
MATERIALS AND METHODS: Male Sprague-Dawley rats received ES-SW (100 and 300 mg/kg, p. o.) for 3 weeks, with DEX (0.5 mg/kg, i. p.) co-administered during the final 2 weeks. Muscle function, muscle mass, and tibialis anterior histomorphometry were assessed. Serum insulin-like growth factor-1 (IGF-1), creatine kinase-MM (CK-MM), and plasma interleukin-6 (IL-6) levels were quantified. In C2C12 myotubes, the effects of ES-SW on DEX-induced (50 μM) atrophy and proteostasis-related signaling pathways were evaluated.
RESULTS: DEX treatment induced a catabolic phenotype characterized by reduced grip strength, muscle mass, and myofiber cross-sectional area, along with decreased IGF-1 and increased CK-MM and IL-6 levels. ES-SW dose-dependently attenuated these functional and structural deteriorations, with the 300 mg/kg group exhibiting the most pronounced protective effects. In skeletal muscle, ES-SW increased the phosphorylation of FoxO3a and suppressed the expression of the atrogenes, muscle atrophy F-box and muscle RING finger-1, and modulated autophagy-associated protein turnover, as reflected by changes in LC3B and p62 expression. In C2C12 myotubes, ES-SW mitigated DEX-induced myotube atrophy and was associated with modulation of FoxO3a and Akt/mTOR signaling.
CONCLUSIONS: Standardized ES-SW effectively attenuated DEX-induced muscle atrophy, accompanied by suppression of FoxO3a-associated atrogene expression, with supportive in vitro evidence suggesting involvement of regulatory pathways associated with muscle protein turnover. These findings support ES-SW as a sustainable ethnopharmacological candidate for the management of glucocorticoid-associated muscle wasting.