Bazi Bushen Attenuates Skeletal Muscle Decline Associated With Oestrogen Deficiency and Modulates FGFR1/ERK Signalling.
7 affiliations
- 1Key Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
- 2Shandong Key Laboratory of Endocrine Metabolism and Aging, Jinan, Shandong, China.
- 3Shandong Institute of Endocrine and Metabolic Diseases, Jinan, Shandong, China.
- 4State Key Laboratory for Innovation and Transformation of Luobing Theory, Hebei Yiling Hospital, Shijiazhuang, Hebei, China.
- 5Shandong Provincial Hospital Affiliated to Shandong First Medical University, "Chuangxin China" Innovation Base of Stem Cell and Gene Therapy for Endocrine Metabolic Diseases, Jinan, Shandong, China.
- 6Shandong Provincial Hospital Affiliated to Shandong First Medical University, Shandong Engineering Laboratory of Prevention and Control for Endocrine and Metabolic Diseases, Jinan, Shandong, China.
- 7Shandong Engineering Research Center of Stem Cell and Gene Therapy for Endocrine and Metabolic Diseases, Jinan, Shandong, China.
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.
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BibTeX
@article{huang2026bazi,
title = {{Bazi Bushen Attenuates Skeletal Muscle Decline Associated With Oestrogen Deficiency and Modulates FGFR1/ERK Signalling.}},
author = {Dezhi Huang and Na Xu and Qi Chu and Zhenhua Jia and Yan Wang and Jin Xu},
journal = {Journal of cellular and molecular medicine},
year = {2026},
month = oct,
doi = {10.1111/jcmm.71407},
url = {https://europepmc.org/article/MED/42961165},
note = {CC BY},
}
RIS
TY - JOUR
TI - Bazi Bushen Attenuates Skeletal Muscle Decline Associated With Oestrogen Deficiency and Modulates FGFR1/ERK Signalling.
AU - Dezhi Huang
AU - Na Xu
AU - Qi Chu
AU - Zhenhua Jia
AU - Yan Wang
AU - Jin Xu
PY - 2026
DA - 2026/10/30
JO - Journal of cellular and molecular medicine
DO - 10.1111/jcmm.71407
UR - https://europepmc.org/article/MED/42961165
AB - 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.
SN - 1582-1838
SN - 1582-4934
ER -