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BACKGROUND: Glucocorticoids (GCs) are used in the treatment of asthma, autoimmune and allergic disease, but long-term GC therapy increased the bone resorption, oxidative stress, inflammation, and impaired bone formation. Aromadendrin is a flavonol (flavonoid) exhibited the potent effect against oxidative stress and inflammatory disease. The aim of the experimental study was to investigate the antiosteoporosis effect of aromadendrin against dexamethasone (DEX) induced osteoporosis (OS) in the rats. MATERIALS AND METHODS: Female Sprague Dawley rats were used in this study and subcutaneous administration of DEX (2.5 mg/kg/day) was used for the induction of OS in the rats. The rats were received the oral administration of aromadendrin (2.5, 5 and 10 mg/kg) and alendronate for 20 weeks. The body weight, organ weight, transverse diameter, bone length, microcomputed tomography (MicroCT) parameters, oxidative stress parameters, inflammatory cytokines, caspase parameters, inflammatory parameters and messenger ribonucleic acid (mRNA) expression were estimated. RESULTS: Aromadendrin treatment improved the body weight and altered the organ weight (vagina, uterus, and femoral weight); bone weight, transverse diameter, bine length, bone mineral density and bone mineral content level. Aromadendrin altered the level of MicroCT parameters, bone parameters (osteocalcin [OC], border gateway protocol, tartrate-resistant acid phosphatase, beta-CrossLaps, alkaline phosphatase, acid phosphatase); nutrient (phosphorus, magnesium, calcium, 1,25(OH)2-vitamin D3); hormone level (calcitonin, parathyroid hormone, E2), oxidative stress, inflammatory cytokines, inflammatory parameters (nuclear factor-κB [NF-κB], C-reactive protein, monocyte chemoattractant protein-1); caspase parameters (caspase-3, caspase-8, caspase-9), receptor activator of nuclear factor B ligand (RANKL), Osteoprotegerin (OPG), and OPG/RANKL ratio, respectively. Aromadendrin treatment altered the mRNA expression of RANKL, OPG, OPG/RANKL ratio. CONCLUSION: Aromadendrin exerts an anti-OS effect against DEX-induced OS in rats via alteration of NF-κB and RANKL/OPG signaling pathway.
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Ma et al. (2026) studied this question.
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