Abstract

In traditional oriental medicines, Commiphora myrrha and its resinous exudate (i.e., myrrh) are used as herbal remedies to treat various inflammatory and metabolic disorders. Until now, C. myrrha-derived herbal products are considered useful source for bioactive compounds to manage numerous human diseases. This study investigated the effects of water extract of C. myrrha resin (WCM) and its polysaccharide (WCM-PE) on modulatory effects of osteoclast differentiation and/or ovariectomized-induced bone loss. Oral administration of WCM (200 and 500 mg/kg/day for four weeks) notably decreased trabecular bone loss and lipid accumulation in the bone marrow cavity. WCM and WCM-PE dose-dependently inhibited receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis and suppressed RANKL-mediated overexpression of c-Fos and nuclear factor of activated T cells, cytoplasmic 1, thereby downregulating osteoclast-specific gene (Atp6v0d2, DC-STAMP and cathepsin K) expression. Thus, our results suggest that WCM and WCM-PE are promising nutraceutical candidates for the management of osteoporosis in postmenopausal women.

Highlights

  • Estrogen deprivation rapidly causes bone loss and porosity via an increase in osteoclast activation, because estrogen is closely implicated in bone turnover and homeostasis [2]

  • These results indicate that osteoporosis-related symptoms due to surgical menopause were successfully induced

  • To the best of our knowledge, this is the first study to demonstrate the protective effects of myrrh and its polysaccharides (i.e., water extract of Commiphora myrrha resin (WCM-PE))

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Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Osteoporosis is an abnormal bone remodeling disease characterized by low bone density and microarchitectural disruption that poses a threat to the elderly as well as menopausal women with excessive osteoclast activation and bone resorption [1]. Estrogen deprivation rapidly causes bone loss and porosity via an increase in osteoclast activation, because estrogen is closely implicated in bone turnover and homeostasis [2]. Osteoclasts derived from monocyte/macrophage lineage cells are unique multinucleated bone-resorbing cells that secrete tartrate-resistant acid phosphatase (TRAP)

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