ArticleJournal of molecular histology2025
Capsaicin counteracts dexamethasone-induced osteoporosis and metabolic disturbances in rats: role of AMPK/SIRT1/β-catenin/RUNX2 pathway.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Given their potent immunosuppressive and anti-inflammatory effects, long-term glucocorticoid therapy (GCs) is a common cause of bone fractures and secondary osteoporosis. Transient receptor potential vanilloid 1 (TRPV1) has been shown to play a role in preserving bone homeostasis and preventing bone disorders. The chili pepper is a naturally occurring source of capsaicin, a TRPV1 agonist. For this reason, this study compared the anti-resorptive properties of capsaicin with alendronate, the conventional treatment for osteoporosis, using a rat model of osteoporosis induced by dexamethasone (Dexa). Over six weeks, five groups of rats received the vehicle, Dexa alone (0.1 mg/kg, Sc), or Dexa plus either alendronate (1 mg/kg, orally) or capsaicin (1 or 2.5 mg/kg, orally). After the experiment, osteocalcin, RANKL, phosphorus, calcium, alkaline phosphatase (ALP), and metabolic parameters were measured. Furthermore, AMPK levels and the relative expression of Bax, Bcl-2, SIRT1, β-catenin, and RUNX2 were assessed in bone, and tissues from the femur were evaluated histologically. Capsaicin's effectiveness in alleviating the bone-damaging effect of dexamethasone was evident through a dose-dependent reduction in ALP, RANKL, and Bax, a rise in osteocalcin and Bcl-2, and a higher expression of AMPK, SIRT1, β-catenin, and RUNX2. Additionally, capsaicin improved bone architecture and effectively mitigated Dexa's detrimental metabolic impact on blood glucose and lipid profile. By upregulating the AMPK/SIRT1/β-catenin/RUNX2 pathway, capsaicin exhibits dose-dependent bone-stimulant effects in a dexamethasone-induced osteoporosis model in rats.
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