N-甲基-D-天冬氨酸受体相关性骨癌痛作用机制研究进展  

Research Progress on Mechanism of N-Methyl-D-Aspartate Receptor-Associated Bone Cancer Pain

作　　者：王陈昆 蒋为薇 WANG Chenkun;JIANG Weiwei(College of Pharmacy,Chongqing Medical University,Chongqing,China 400016;The Second Affiliated Hospital of Chongqing Medical University,Chongqing,China 400010)

机构地区：[1]重庆医科大学药学院,重庆400016 [2]重庆医科大学附属第二医院,重庆400010

出　　处：《中国药业》2022年第21期128-128,I0001-I0007,共8页China Pharmaceuticals

摘　　要：目的探讨N-甲基-D-天冬氨酸(NMDA)受体相关性骨癌痛的作用机制。方法检索国内外相关文献,从NMDA受体及其亚基NR1和NR2B,以及NMDA相关性通路方面进行总结与分析。结果作用机制包括驱动蛋白家族KIF17介导的NR2B树突转运,炎性因子诱导NMDA受体亚基磷酸化,以及含NR2B的NMDA受体-Ca^(2+)/Ca^(2+)-钙调蛋白依赖性蛋白激酶Ⅱ(CaMKⅡ)-环磷酰腺苷反应元件结合蛋白(CREB)-CREB转录共激活因子1(CRTC1)-脑源性神经营养因子(BDNF)-NR2B的正反馈通路。结论相关研究可为骨癌痛的镇痛治疗提供新的参考靶点,同时也为临床骨癌痛的镇痛治疗提供了参考。Objective To investigate the mechanism of N-methyl-D-aspartate(NMDA)receptor-associated bone cancer pain(BCP).Methods The related studies at home and abroad were searched,and the related information of NMDA receptor,its subunits including NR1 and NR2B,the NMDA-associated pathways were summarized and analyzed.Results The mechanisms of NMDA receptor-associated BCP included the dendrite transport of NR2B mediated by the kinesin family member 17(KIF17),the phosphorylation of NMDA receptor subunits induced by inflammatory cytokines,and the positive feedback pathway of NMDA receptor containing NR2B-Ca^(2+)/Ca^(2+)-calmodulin-dependent protein kinaseⅡ(CaMKⅡ)-cAMP-response element binding protein(CREB)-CREB-regulated transcription coactivator 1(CRTC1)-brain-derived neurotrophic factor(BDNF)-NR2B.Conclusion Related researches can provide a reference for the new targets of analgesic treatment of BCP and the clinical analgesic treatment of BCP.

关 键 词：骨癌痛 N-甲基-D-天冬氨酸受体 NR1亚基 NR2B亚基 环磷酰腺苷反应元件结合蛋白 KIF17 炎性因子 进展 

分 类 号：R965[医药卫生—药理学] R730.6[医药卫生—药学]