Molecular biology reports · 2026
Combined metformin and Taurine attenuate age-related bone loss.
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Zhao Jun, Shi Wentao, Wang Juan, Que Yunduan, Lv Long, Chen Changsheng
Аннотация
BACKGROUND: Age-related bone loss is closely associated with functional decline and exhaustion of bone marrow mesenchymal stem cells (BMSCs). This study aimed to investigate whether combined Metformin and Taurine (Met + Ta) treatment could attenuate aging-associated skeletal deterioration and preserve BMSC function.
METHODS: Eighteen-month-old male C57BL/6J mice were treated with Met, Ta, or Met + Ta for 8 consecutive weeks. Bone microarchitecture was evaluated by micro-computed tomography and histological staining. BMSCs were isolated from aged mice and assessed for osteogenic differentiation, proliferative capacity, senescence-related changes, and inflammatory cytokine production. Transcriptomic analysis was performed to identify molecular changes associated with Met + Ta treatment, and siRNA-mediated Crebrf knockdown was used for functional validation.
RESULTS: Met + Ta treatment improved bone mass and trabecular microarchitecture more effectively than either single treatment. Histological staining further showed better preservation of trabecular structure and increased collagen-rich matrix deposition in the Met + Ta group. BMSCs from Met + Ta-treated mice exhibited enhanced osteogenic differentiation, increased proliferative activity, reduced senescence-associated phenotypes, and improved inflammatory homeostasis. Transcriptomic analysis revealed coordinated regulation of genes involved in proliferation, senescence, metabolism, proteostasis, and genome maintenance. Crebrf was identified as a candidate regulatory mediator, and Crebrf knockdown attenuated the anti-senescent and cellular-stability-related effects of Met + Ta in BMSCs.
CONCLUSIONS: Combined Met and Ta treatment alleviates age-related bone loss and preserves BMSC function more effectively than single-agent treatment. These findings suggest that Met + Ta may represent a potential combined strategy for delaying skeletal aging, with Crebrf serving as a candidate mediator of its protective effects.
METHODS: Eighteen-month-old male C57BL/6J mice were treated with Met, Ta, or Met + Ta for 8 consecutive weeks. Bone microarchitecture was evaluated by micro-computed tomography and histological staining. BMSCs were isolated from aged mice and assessed for osteogenic differentiation, proliferative capacity, senescence-related changes, and inflammatory cytokine production. Transcriptomic analysis was performed to identify molecular changes associated with Met + Ta treatment, and siRNA-mediated Crebrf knockdown was used for functional validation.
RESULTS: Met + Ta treatment improved bone mass and trabecular microarchitecture more effectively than either single treatment. Histological staining further showed better preservation of trabecular structure and increased collagen-rich matrix deposition in the Met + Ta group. BMSCs from Met + Ta-treated mice exhibited enhanced osteogenic differentiation, increased proliferative activity, reduced senescence-associated phenotypes, and improved inflammatory homeostasis. Transcriptomic analysis revealed coordinated regulation of genes involved in proliferation, senescence, metabolism, proteostasis, and genome maintenance. Crebrf was identified as a candidate regulatory mediator, and Crebrf knockdown attenuated the anti-senescent and cellular-stability-related effects of Met + Ta in BMSCs.
CONCLUSIONS: Combined Met and Ta treatment alleviates age-related bone loss and preserves BMSC function more effectively than single-agent treatment. These findings suggest that Met + Ta may represent a potential combined strategy for delaying skeletal aging, with Crebrf serving as a candidate mediator of its protective effects.