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Войти в исследования Experimental gerontology · 2025
Therapeutic effects of Total flavonoids of Epimedium Folium on sarcopenia via modulation of gut microbiota and bile acid metabolism.
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Zhang Yujie, Pan Zhe, Shi Jiewen, Zhang Jingjing, Chai Yongli, Zhao Ye, Liu Wei, Yuan Wei''an
Аннотация
BACKGROUND: The total flavonoids of Epimedii Folium (Epimedium brevicornu Maxim.) are the main active component, and have unique advantages in sarcopenia intervention. Nevertheless, its efficacy and mechanism of action have not been reported in the literature.
AIM OF THE STUDY: This study aimed to evaluate the impact of TFE on sarcopenia and to elucidate the mechanisms involving the FXR-FGF15 signaling pathway and the gut microbiota-bile acid-skeletal muscle axis.
METHODS: At the cellular level, the effects of TFE on C2C12 myotube morphology, as well as on myogenic growth factors and atrophy-related markers, were evaluated. At the animal level, the effects of TFE on sarcopenia were investigated through assessments of senescence score, grip strength, body composition, running performance, and histological analysis of skeletal muscle tissue. The levels of inflammatory cytokines in serum were assayed using ELISA to assess the inflammation. Pyrosequencing of bacterial 16S rRNA from the V3-V4 of fecal samples characterized the gut microbiota. Targeted bile acid metabolomics in fecal and skeletal muscle samples were measured using UHPLC-Q-Exactive Orbitrap HRMS. qRT-PCR and western blot were used to evaluate markers related to bile acid synthesis, transport, and absorption, as well as the FXR-FGF15 signaling pathway.
RESULTS: TFE helps prevent dexamethasone-induced muscle atrophy and degeneration by upregulating the expression of myogenic growth factors (MyoD, Mef2a, and MyoG) and downregulating the expression of muscle atrophy markers (Trim63, Fbxo32). 12 weeks TFE administration has significant therapeutic properties in SAMP8 mice, as demonstrated by lower senescence score and body fat content; greater grip force, lean muscle content and muscle function (running time and distance), and have the effects of delaying the progression of aging and repairing the pathological damage of skeletal muscle in the SAMP8 mice. Its mechanism of action may involve restoring gut microbiota imbalance and bile acid metabolism disruption, thereby positively regulating FXR-FGF15 signaling.
CONCLUSIONS: In the present study, TFE was shown to improve dexamethasone-induced muscle atrophy and degeneration in C2C12 myotubes, as evidenced by the restored expression of myogenic markers and the downregulation of atrophy-related genes and proteins. Additionally, TFE can attenuate sarcopenia progression in SAMP8 mice. Its effect was related to the regulation of the gut microbiota-bile acids-skeletal muscle axis.
AIM OF THE STUDY: This study aimed to evaluate the impact of TFE on sarcopenia and to elucidate the mechanisms involving the FXR-FGF15 signaling pathway and the gut microbiota-bile acid-skeletal muscle axis.
METHODS: At the cellular level, the effects of TFE on C2C12 myotube morphology, as well as on myogenic growth factors and atrophy-related markers, were evaluated. At the animal level, the effects of TFE on sarcopenia were investigated through assessments of senescence score, grip strength, body composition, running performance, and histological analysis of skeletal muscle tissue. The levels of inflammatory cytokines in serum were assayed using ELISA to assess the inflammation. Pyrosequencing of bacterial 16S rRNA from the V3-V4 of fecal samples characterized the gut microbiota. Targeted bile acid metabolomics in fecal and skeletal muscle samples were measured using UHPLC-Q-Exactive Orbitrap HRMS. qRT-PCR and western blot were used to evaluate markers related to bile acid synthesis, transport, and absorption, as well as the FXR-FGF15 signaling pathway.
RESULTS: TFE helps prevent dexamethasone-induced muscle atrophy and degeneration by upregulating the expression of myogenic growth factors (MyoD, Mef2a, and MyoG) and downregulating the expression of muscle atrophy markers (Trim63, Fbxo32). 12 weeks TFE administration has significant therapeutic properties in SAMP8 mice, as demonstrated by lower senescence score and body fat content; greater grip force, lean muscle content and muscle function (running time and distance), and have the effects of delaying the progression of aging and repairing the pathological damage of skeletal muscle in the SAMP8 mice. Its mechanism of action may involve restoring gut microbiota imbalance and bile acid metabolism disruption, thereby positively regulating FXR-FGF15 signaling.
CONCLUSIONS: In the present study, TFE was shown to improve dexamethasone-induced muscle atrophy and degeneration in C2C12 myotubes, as evidenced by the restored expression of myogenic markers and the downregulation of atrophy-related genes and proteins. Additionally, TFE can attenuate sarcopenia progression in SAMP8 mice. Its effect was related to the regulation of the gut microbiota-bile acids-skeletal muscle axis.