解放军医学院学报
解放軍醫學院學報
해방군의학원학보
Academic Journal of Chinese Pla Medical School
2015年
4期
396-398
,共3页
邱方%刘艳红%米卫东%李泱
邱方%劉豔紅%米衛東%李泱
구방%류염홍%미위동%리앙
趋化因子%疼痛%受体%伤害感受
趨化因子%疼痛%受體%傷害感受
추화인자%동통%수체%상해감수
chemokines%pain%receptors%nociception
趋化因子配体12(CXC-chemokine ligand 12,CXCL12),也被称为基质细胞源性因子(stromal cell-derived factor 1, SDF-1),是在免疫系统中被发现的趋化因子,它的主要功能包括趋化淋巴细胞和巨噬细胞、负责造血细胞从肝向骨髓的迁移以及大血管的形成。越来越多的证据表明,外周神经系统中神经组织或非神经组织上疾病相关或者损伤相关的SDF-1及其受体-趋化因子受体4(CXC-chemokine receptor 4,CXCR4)的功能性表达,在慢性疼痛的病理生理过程中发挥了重要的作用。生理状态下,SDF-1可以作为中枢神经系统中经典的神经调质,调节神经内分泌网络的活动。病理状态下(改变的免疫反应和炎症状态下),由于胶质细胞、内皮细胞的分泌以及循环系统的运输,SDF-1浓度会增加或者在异常部位表达,从而影响神经内分泌活动,改变大脑的功能,导致病理性行为和神经毒性。综上所述,SDF-1/CXCR4是未来新药开发的潜在靶点。
趨化因子配體12(CXC-chemokine ligand 12,CXCL12),也被稱為基質細胞源性因子(stromal cell-derived factor 1, SDF-1),是在免疫繫統中被髮現的趨化因子,它的主要功能包括趨化淋巴細胞和巨噬細胞、負責造血細胞從肝嚮骨髓的遷移以及大血管的形成。越來越多的證據錶明,外週神經繫統中神經組織或非神經組織上疾病相關或者損傷相關的SDF-1及其受體-趨化因子受體4(CXC-chemokine receptor 4,CXCR4)的功能性錶達,在慢性疼痛的病理生理過程中髮揮瞭重要的作用。生理狀態下,SDF-1可以作為中樞神經繫統中經典的神經調質,調節神經內分泌網絡的活動。病理狀態下(改變的免疫反應和炎癥狀態下),由于膠質細胞、內皮細胞的分泌以及循環繫統的運輸,SDF-1濃度會增加或者在異常部位錶達,從而影響神經內分泌活動,改變大腦的功能,導緻病理性行為和神經毒性。綜上所述,SDF-1/CXCR4是未來新藥開髮的潛在靶點。
추화인자배체12(CXC-chemokine ligand 12,CXCL12),야피칭위기질세포원성인자(stromal cell-derived factor 1, SDF-1),시재면역계통중피발현적추화인자,타적주요공능포괄추화림파세포화거서세포、부책조혈세포종간향골수적천이이급대혈관적형성。월래월다적증거표명,외주신경계통중신경조직혹비신경조직상질병상관혹자손상상관적SDF-1급기수체-추화인자수체4(CXC-chemokine receptor 4,CXCR4)적공능성표체,재만성동통적병리생리과정중발휘료중요적작용。생리상태하,SDF-1가이작위중추신경계통중경전적신경조질,조절신경내분비망락적활동。병리상태하(개변적면역반응화염증상태하),유우효질세포、내피세포적분비이급순배계통적운수,SDF-1농도회증가혹자재이상부위표체,종이영향신경내분비활동,개변대뇌적공능,도치병이성행위화신경독성。종상소술,SDF-1/CXCR4시미래신약개발적잠재파점。
The chemokine CXCL12/stromal cell-derived factor 1 (SDF-1) is one of the chemokines that have been described in immune system. Its main functions include chemotaxis for lymphocytes and macrophages, migration of hematopoietic cells from fetal liver to bone marrow and the formation of large blood vessels. Accumulating evidences indicate that disease associated or injury-induced functional expression of CXCL12/CXCR4 signaling in both neural and non-neural elements of peripheral nervous system play important roles in the pathophysiology of chronic pain. Under normal conditions, CXCL12 can also act in central nerve system (CNS) as a classical neuromediator and can modulate the activity of several neuroendocrine networks. However, during pathological state (altered immune response or inflammation), due to its local production by glial and/or endothelial cells and/or its diffusion and transportation through the vascular circulation, enhanced concentrations of CXCL12 and/or its presence at unusual sites can affect neuronal and neuroendocrine activities and modify the functioning of the brain, leading to pathological behaviors and/or neurotoxicity. In conclusion, CXCL12/CXCR4 signaling is a potential target for the development of novel therapeutics.