COX-2与骨代谢关系的研究进展  

Research progress of the relationship between COX-2 and bone formation

作　　者：马吴迪[1] 夏伦果[1] 周宇宁 徐袁瑾[1] 

机构地区：[1]上海交通大学医学院附属第九人民医院.口腔医学院口腔外科上海市口腔医学重点实验室,上海20011

出　　处：《中国口腔颌面外科杂志》2016年第1期83-88,共6页China Journal of Oral and Maxillofacial Surgery

摘　　要：环氧化酶2(cyclooxygenase-2,COX-2)是花生四烯酸(arachidonic acid,AA)合成前列腺素E2(prostaglandin E2,PGE2)的限速酶,通过对PGE2的调控,COX-2能够对骨代谢中骨形成和骨吸收产生多种不同的作用。同时,COX-2也能通过参与多条信号转导途径,影响骨的形成,包括G蛋白α亚基(guanine nucleotide-binding proteins alpha s,Gαs)信号通路、促丝裂原激活蛋白激酶(mitogen-activated protein kinases,MAPKs)通路以及核因子受体激活物配基(receptor activator of nuclear factorκB ligand,RANKL)信号通路。COX-2的产生由多种因素诱导,并可被其抑制剂如非甾体类抗炎药(non-steroidal anti-inflammatory drugs,NSAID)抑制。这些因素能调控COX-2的产量并最终作用于骨组织。本文就COX-2与骨形成的关系及其在相关临床应用上的展望进行介绍。[Summary] Cyelooxygenase-2 （COX-2） is the rate-limiting enzyme of arachidonic acid （AA） synthesizing prostaglandin E2 （PGE2）. It has various effects on bone metabolism that stimulate both bone resorption and formation through regulation of PGE2. Meanwhile, COX-2 can work by the participation of multiple signal transduction pathways in bone formation, including Gcts signaling pathway, mitogen-activated protein kinases （MAPKs） pathway and receptor activator of nuclear factor KB ligand （RANKL） signaling pathway. COX-2 was induced by many factors, and can be inhibited by the inhibitors such as non-steroidal anti-inflammatory drugs （NSAIDs）. These factors can regulate the production of COX-2 and consequently have impact on bone tissue. The main purpose of the article was to introduce the relationship between COX- 2 and bone formation and its potential clinical applications.

关 键 词：环氧化酶2 前列腺素 骨形成 成骨细胞 破骨细胞 

分 类 号：R580[医药卫生—内分泌]