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Formononetin attenuates osteoclast differentiation and calcium loss by mediating transcription factor AP-1 in type I
Wensen Jing1, Lei Feng1, Kan Peng1
1Department of Joint Surgery, Honghui Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Abstract:
Formononetin (FMN) has been reported as a prospective antiosteoporotic medication. However, the antiosteoporotic properties of FMN are still unclear in a mouse model with diabetes-induced osteoporosis. An osteoporotic or osteopenic mouse model with type I diabetes mellitus (T1DM) was established using streptozotocin (40 mg/kg) injection for 5 consecutive days. After 12 weeks with FMN intragastric administration (0.5, 5, 20 mg/kg), the antiosteoporotic activity of FMN was evaluated in T1DM mice. FMN supplementation effectively improves Ca excretion and trabecular bone degeneration and impedes osteoclast differentiation and function to attenuate hyperglycemia-induced bone deterioration. In addition, FMN inhibited activating protein 1 (AP-1) and osteoclast-specific gene expression, Nfatc1, Ctsk, and TRAP. The administration of FMN has a beneficial effect to attenuate hyperglycemia-induced bone deteriorations, including osteoclastogenesis, trabecular bone, and Ca loss. Our study provided a prospective medication for the treatment of T1DM-related osteopenia or osteoporosis with FMN.
Insights
Formononetin (FMN) shows promise in treating osteoporosis linked to type I diabetes mellitus (T1DM). This study found FMN improves bone density and reduces bone loss in a T1DM mouse model.
Area of Science:
- Endocrinology
- Bone Biology
- Pharmacology
Background:
- Type I diabetes mellitus (T1DM) often leads to osteopenia and osteoporosis.
- The antiosteoporotic effects of Formononetin (FMN) in T1DM-induced bone loss are not well understood.
Purpose of the Study:
- To investigate the efficacy of Formononetin (FMN) in ameliorating bone deterioration in a mouse model of type I diabetes mellitus (T1DM)-induced osteoporosis.
Main Methods:
- An osteoporotic mouse model was established using streptozotocin injection.
- Mice received intragastric administration of FMN (0.5, 5, 20 mg/kg) for 12 weeks.
- Evaluated FMN's impact on calcium excretion, bone structure, and osteoclast activity.
Main Results:
- FMN treatment improved calcium excretion and reduced trabecular bone degeneration.
- FMN effectively inhibited osteoclast differentiation and function.
- FMN suppressed the expression of AP-1, Nfatc1, Ctsk, and TRAP genes.
Conclusions:
- Formononetin (FMN) demonstrates significant potential in mitigating hyperglycemia-induced bone deterioration in T1DM.
- FMN administration offers a beneficial therapeutic strategy for T1DM-related osteopenia and osteoporosis.
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