Magnolol prevents ovariectomy‑induced bone loss by suppressing osteoclastogenesis via inhibition of the nuclear factor‑κB and mitogen‑activated protein kinase pathways.

Abstract

Magnolol is the active component of the traditional Chinese medicine Magnolia officinalis, and has antioxidant, anti-inflammatory and anticancer activities, as well as an effect on bone metabolism in vitro. In the present study, it is reported that magnolol suppresses osteoclastogenesis in vivo and in vitro. Magnolol prevented ovariectomy-induced bone loss and osteoclastogenesis in vivo, and decreased the serum levels of C-terminal telopeptide of type 1 collagen, interleukin-6, tumor necrosis factor (TNF)-α and tartrate-resistant acid phosphatase 5B. In vitro, magnolol inhibited the osteoclastogenesis induced by the receptor activator for nuclear factor-κB ligand, and impaired the osteoclast function in bone marrow monocytes and RAW264.7 cells in a dose-dependent manner. Furthermore, magnolol suppressed the expression levels of the osteoclastogenesis markers cathepsin K, calcitonin receptor, matrix metalloproteinase 9, TNF receptor-associated factor 6 and tartrate-resistant acid phosphatase by inhibiting the nuclear factor-κB and mitogen-activated protein kinase pathways. Therefore, magnolol is a promising agent for the treatment of osteoporosis and associated disorders.