Effect of Ellipticine in Glucocorticoid-Induced Osteoporosis: In Silico and In Vivo Analyses

Glucocorticoids cause secondary osteoporosis, which leads to considerable morbidity from fractures. The antiosteoporosis activity of ellipticine against glucocorticoid-induced osteoporosis in rats was investigated in the present study. Sprague-Dawley rats were used and dexamethasone (2.5 mg/kg) was used to induce osteoporosis, after which the rats were given ellipticine (test sample) and alendronate (positive control) for 20 weeks. Bone turnover, antioxidants, inflammatory cytokines, nutritional parameters, and hormone factors were variables measured. Ellipticine reduced body weight and considerably increased uterine and vaginal weight. Ellipticine dramatically increased trabecular bone number levels while suppressing bone volume fraction, trabecular separation, bone surface fraction, and trabecular thickness. Ellipticine raised circulatory osteocalcin levels while decreasing bone Gla protein, acid phosphatase, alkaline phosphatase, and beta-C-terminal telopeptide levels considerably. Ellipticine increased serum malonyl dialdehyde levels while decreasing plasma glutathione, catalase, and superoxide dismutase levels, as well as suppressing inflammatory cytokines. Ellipticine significantly reduced potassium, calcium, 25(OH)vitamin D and magnesium levels and increased estradiol levels while suppressing parathyroid hormone and tartrate-resistant acid phosphatase levels. Ellipticine reduced the level of receptor activator of nuclear factor-kappa B ligand while increasing the level of osteoprotegerin. Docking study demonstrated that ellipticine docked the estrogen receptors (alpha and beta) and VDR (vitamin D receptor). Consequently, ellipticine exhibited antiosteoporosis effects against glucocorticoid-induced loss of bone in rats.