Oral compound ossotide prevents bone destruction in retinoic acid-induced mice osteoporosis model

Osteoporosis (OP) is a systemic metabolic bone disease characterized by the reduction of bone mineral density (BMD). In clinic, reversing the decreasing of BMD is the main therapeutic strategy of OP, including estrogen, bisphosphonates, calcium supplements, flavonoids, Vitamin D and anabolic steroids, however, serious side effects limit their application. Herein, the compound ossotide, derived from porcine bone and scorpions, can significantly enhance the BMD via oral administration in retinoic acid-induced mice osteoporosis model and down-regulate the expression of serum calcium, phosphorus, BALP, TRAP and OCN, up-regulate the serum TGF-β expression. The mechanism studies showed that compound ossotide could promote the proliferation and differentiation of osteoblasts by up-regulating Runx2 and OPG/RANKL expression ratio. Besides, compound ossotide can inhibit RANKL-induced osteoclast differentiation and the transcriptional activation of NFATc1. The results indicate that compound ossotide can be used as an efficient candidate for OP treatment via oral administration.