Journal of ethnopharmacology · 2026
Albiflorin attenuates dexamethasone-induced muscle atrophy by suppressing catabolic signaling and enhancing myogenic differentiation.
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Kim Minsun, Kim Jae-Hyun, Lee Sumin, Shin Won Jeong, Kim Eom Ji, Park Hoyeon, Park Jae Ho, Kim Eun-Young, Jung Hyuk-Sang, Sohn Youngjoo
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Paeonia lactiflora Pall. Has been widely used in East Asian traditional medicine for the treatment of inflammatory disorders and muscle-related conditions. Albiflorin, a monoterpene glycoside derived from this herb, is considered one of its principal bioactive constituents; however, its potential role in skeletal muscle atrophy has not been fully elucidated.
AIM OF THE STUDY: This study aimed to investigate the protective effects of albiflorin against dexamethasone-induced muscle atrophy and to elucidate the underlying molecular mechanisms.
MATERIALS AND METHODS: The anti-atrophic effects of albiflorin were evaluated in differentiated C2C12 myotubes and a dexamethasone-induced mouse model. Cell viability, myotube morphology, and expression of muscle atrophy-related and myogenic regulatory factors were analyzed. In vivo, body weight, grip strength, muscle thickness, histological changes, and serum biochemical parameters were assessed.
RESULTS: Albiflorin significantly attenuated dexamethasone-induced cytotoxicity and myotube atrophy in C2C12 cells. It suppressed the expression of muscle-specific E3 ubiquitin ligases MuRF1 and MAFbx and increased Akt phosphorylation, while enhancing the expression of myogenic markers including MyoD and Myogenin. In the mouse model, albiflorin preserved body weight, grip strength, and gastrocnemius muscle thickness, increased muscle fiber cross-sectional area and density, and improved serum biochemical markers, including AST, ALT, and lactate dehydrogenase, along with partial restoration of insulin-like growth factor-1.
CONCLUSION: Albiflorin exerts protective effects against dexamethasone-induced muscle atrophy by suppressing catabolic signaling and promoting myogenic differentiation. These findings provide experimental evidence supporting the traditional use of Paeonia lactiflora in muscle-related conditions and suggest its potential relevance in the management of muscle wasting disorders.
AIM OF THE STUDY: This study aimed to investigate the protective effects of albiflorin against dexamethasone-induced muscle atrophy and to elucidate the underlying molecular mechanisms.
MATERIALS AND METHODS: The anti-atrophic effects of albiflorin were evaluated in differentiated C2C12 myotubes and a dexamethasone-induced mouse model. Cell viability, myotube morphology, and expression of muscle atrophy-related and myogenic regulatory factors were analyzed. In vivo, body weight, grip strength, muscle thickness, histological changes, and serum biochemical parameters were assessed.
RESULTS: Albiflorin significantly attenuated dexamethasone-induced cytotoxicity and myotube atrophy in C2C12 cells. It suppressed the expression of muscle-specific E3 ubiquitin ligases MuRF1 and MAFbx and increased Akt phosphorylation, while enhancing the expression of myogenic markers including MyoD and Myogenin. In the mouse model, albiflorin preserved body weight, grip strength, and gastrocnemius muscle thickness, increased muscle fiber cross-sectional area and density, and improved serum biochemical markers, including AST, ALT, and lactate dehydrogenase, along with partial restoration of insulin-like growth factor-1.
CONCLUSION: Albiflorin exerts protective effects against dexamethasone-induced muscle atrophy by suppressing catabolic signaling and promoting myogenic differentiation. These findings provide experimental evidence supporting the traditional use of Paeonia lactiflora in muscle-related conditions and suggest its potential relevance in the management of muscle wasting disorders.