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Oridonin ameliorates inflammation-induced bone loss in mice via suppressing DC-STAMP expression

	author = {Bin-hua Zou and Yan-hui Tan and Wen-de Deng and Jie-huang Zheng and Qin Yang and Min-hong Ke and Zong-bao Ding and Xiao-juan Li},
	title = {Oridonin ameliorates inflammation-induced bone loss in mice via suppressing DC-STAMP expression},
	journal = {Acta Pharmacologica Sinica},
	volume = {42},
	number = {5},
	year = {2021},
	keywords = {},
	abstract = {Currently, dendritic cell-specific transmembrane protein (DC-STAMP), a multipass transmembrane protein, is considered as the master regulator of cell–cell fusion, which underlies the formation of functional multinucleated osteoclasts. Thus, DC-STAMP has become a promising target for osteoclast-associated osteolytic diseases. In this study, we investigated the effects of oridonin (ORI), a natural tetracyclic diterpenoid compound isolated from the traditional Chinese herb Rabdosia rubescens, on osteoclastogenesis in vivo and ex vivo. ICR mice were injected with LPS (5 mg/kg, ip, on day 0 and day 4) to induce inflammatory bone destruction. Administration of ORI (2, 10 mg·kg−1·d−1, ig, for 8 days) dose dependently ameliorated inflammatory bone destruction and dramatically decreased DC-STAMP protein expression in BMMs isolated from LPS-treated mice. Treatment of preosteoclast RAW264.7 cells with ORI (0.78–3.125 μM) dose dependently inhibited both mRNA and protein levels of DC-STAMP, and suppressed the following activation of NFATc1 during osteoclastogenesis. Knockdown of DC-STAMP in RAW264.7 cells abolished the inhibitory effects of ORI on RANKL-induced NFATc1 activity and osteoclast formation. In conclusion, we show for the first time that ORI effectively attenuates inflammation-induced bone loss by suppressing DC-STAMP expression, suggesting that ORI is a potential agent against inflammatory bone diseases.},
	issn = {1745-7254},	url = {}