Idris Aymen I, van 't Hof Robert J, Greig Iain R, Ridge Susan A, Baker David, Ross Ruth A, Ralston Stuart H
Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK.
Nat Med. 2005 Jul;11(7):774-9. doi: 10.1038/nm1255. Epub 2005 May 22.
Accelerated osteoclastic bone resorption has a central role in the pathogenesis of osteoporosis and other bone diseases. Identifying the molecular pathways that regulate osteoclast activity provides a key to understanding the causes of these diseases and to the development of new treatments. Here we show that mice with inactivation of cannabinoid type 1 (CB1) receptors have increased bone mass and are protected from ovariectomy-induced bone loss. Pharmacological antagonists of CB1 and CB2 receptors prevented ovariectomy-induced bone loss in vivo and caused osteoclast inhibition in vitro by promoting osteoclast apoptosis and inhibiting production of several osteoclast survival factors. These studies show that the CB1 receptor has a role in the regulation of bone mass and ovariectomy-induced bone loss and that CB1- and CB2-selective cannabinoid receptor antagonists are a new class of osteoclast inhibitors that may be of value in the treatment of osteoporosis and other bone diseases.
破骨细胞介导的骨吸收加速在骨质疏松症和其他骨疾病的发病机制中起核心作用。确定调节破骨细胞活性的分子途径是理解这些疾病病因以及开发新治疗方法的关键。在此我们表明,1型大麻素(CB1)受体失活的小鼠骨量增加,并且免受卵巢切除诱导的骨质流失影响。CB1和CB2受体的药理学拮抗剂在体内预防了卵巢切除诱导的骨质流失,并通过促进破骨细胞凋亡和抑制几种破骨细胞存活因子的产生在体外导致破骨细胞抑制。这些研究表明,CB1受体在骨量调节和卵巢切除诱导的骨质流失中起作用,并且CB1和CB2选择性大麻素受体拮抗剂是一类新的破骨细胞抑制剂,可能在骨质疏松症和其他骨疾病的治疗中有价值。