Adrenomedullin inhibits osteoclast differentiation through the suppression of receptor activator of nuclear factor-κB ligand-induced nuclear factor-κB activation in glucocorticoid-induced osteoporosis.

The current study aimed to improve the understanding on the association between adrenomedullin and osteoporosis in mice with glucocorticoid-induced osteoporosis. Bone resorption and osteoporosis-associated indexes, including maximum load, stiffness, energy to failure, ultimate strength, elastic modulus, post-yield displacement and post-yield displacement, in mice with osteoporosis were analyzed in order to evaluate the effect of adrenomedullin. The receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation was investigated subsequent to treatment with adrenomedullin . The results demonstrated that adrenomedullin significantly improved bone mass loss, density, bone strength and osteoporosis disease in the mice with glucocorticoid-induced osteoporosis. In addition, adrenomedullin markedly improved the osteoporosis-associated NFATc1, TRAP, OSCAR and c-Fos expression levels. Furthermore, the current findings indicated that RANKL-mediated osteoclast differentiation was suppressed and . Notably, the data revealed that adrenomedullin significantly improved the osteoporotic symptoms through inhibition of RANKL-induced NF-κB activation in glucocorticoid-induced osteoporosis. In conclusion, adrenomedullin serves an essential role in the progression of glucocorticoid-induced osteoporosis, regulating the bone mass loss, density and strength through the NF-κB signaling pathway.