Authors
Dezhi Huang, Na Xu, Qi Chu, Zhenhua Jia, Yan Wang, Jin Xu
Published in
Journal of cellular and molecular medicine. Volume 30. Issue 21.
Abstract
Postmenopausal oestrogen deficiency is associated with skeletal muscle loss and functional decline, thereby increasing the risk of sarcopenia in women. Considering the safety risks linked to hormone replacement therapy (HRT), alternative strategies are needed to attenuate skeletal muscle decline after menopause. A total of 24 female C57BL/6J mice were randomly assigned to four groups (n = 6 per group): Sham-operated (SHAM), ovariectomized (OVX), OVX treated with estradiol valerate (OVX + E2) and OVX treated with Bazi Bushen (OVX + BZBS). Skeletal muscle mass and function were evaluated in four groups. RNA sequencing was applied to explore the molecular mechanisms and key signalling pathways underlying BZBS-induced muscle protection. We further examined the role of the FGFR1/ERK signalling pathway in mediating the effects of BZBS on myogenic differentiation in C2C12 myoblasts. The results showed that OVX mice had reduced grip strength and skeletal muscle mass, increased fat accumulation, reduced lean mass and impaired metabolic activity. These phenotypic alterations were accompanied by myofiber atrophy, increased collagen staining, endocrine perturbations and elevated expression of p16, p21, Atrogin-1 and MuRF1. BZBS ameliorated these abnormalities. RNA-seq suggested that FGF/MAPK signalling may be involved. In D-gal-treated C2C12 myoblasts, BZBS reduced Atrogin-1 and MuRF1 expression while restoring MYHC and MYOG expression. Mechanistically, BZBS suppressed FGFR1/ERK signalling activation and bFGF partially reversed the protective effects of BZBS. Taken together, these findings suggest that FGFR1/ERK signalling may contribute to the protective effects of BZBS. Our findings provide evidence for the beneficial effects of BZBS on skeletal muscle deterioration associated with oestrogen deficiency.
PMID:
42961165
Bibliographic data and abstract were imported from PubMed on 30 Oct 2026.
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