趋化因子CX3CL1对β-淀粉样蛋白1-42激活的小胶质细胞IL-1β、TNF-α和NO表达的影响  

Effects of CX3CL1 on the expression of inflammatory substances in β-amyloid peptide-activated microglia

作　　者：宋艳芳[1] 林青[1] 周子鑫[1] 高芳琳[1] 陈蓉艳[1] 祝先进[2] SONG Yanfang LIN Qing ZHOU Zixing GAO Fanglin CHEN Rongyan ZHU Xianjin(Department of Laboratory, Fujian Province People＇ s Hospital Affiliated to Fujian College of Traditional Chinese Medicine, Fuzhou 350004, China Department of Laboratory, Union Hospital Affiliated to Fujian Medical University, Fuzhou 350001, China)

机构地区：[1]福建中医药大学附属人民医院检验科,福州350004 [2]福建医科大学附属协和医院检验科,福州350001

出　　处：《免疫学杂志》2016年第12期1101-1104,共4页Immunological Journal

基　　金：福建省自然科学基金(2015J01400;2016J01569)

摘　　要：目的探讨趋化因子CX3CL1对β-淀粉样蛋白1-42(β-amyloid peptide1-42,Aβ1-42)激活的小鼠小胶质细胞(N9)分泌TNF-α、IL-1β和一氧化氮(NO)的影响。方法用一定质量浓度的CX3CL1作用于经Aβ1-42激活的小鼠小胶质细胞,收集细胞培养上清,通过一氧化氮(NO)试剂盒检测培养上清中NO浓度的变化,利用ELISA法检测培养上清中TNF-α和IL-1β质量浓度的变化。结果与对照组相比,Aβ1-42能够明显上调小胶质细胞TNF-α、IL-1β和NO的表达,且具有剂量依赖性;其中,Aβ1-42浓度为10μmol/L时,IL-1β、TNF-α、NO的表达量均达到最高,与对照组(未用Aβ1-42干预)相比,分别升高约2倍、13倍、9倍,差异具有统计学意义(P<0.05);趋化因子CX3CL1能够明显降低Aβ1-42诱导的小胶质细胞TNF-α、IL-1β和NO的表达量,分别下降了约38%、24%、45%,且差异有统计学意义(P<0.05)。结论趋化因子CX3CL1对Aβ1-42激活的小胶质细胞产生的TNF-α、IL-1β和NO的表达具有抑制效应,提示趋化因子CX3CL1可能通过抗炎作用而对神经系统具有保护作用。This study performed to investigate the effects of CX3CL1 on the expression of the tumor necrosisfactor-α（TNF-α）, interlenkin-1β（IL-1β）, and nitric oxide（NO） in β-amyloid peptide-activated murine microgliacells line N9. Microglia cells were pretreated CX3CL1 for 2 h, and then stimulated with Aβ1-42 for 24 h, and thesupernatants were analyzed for IL-1β and TNF-α production by ELISA. The level of NO in the culture supernatantswere detected by the NO test assay. Data showed that the levels of TNF-α, IL-1β and NO in the culturesupernatants evidently increased in Aβ1-42-activated microglia cells in a dose-dependent manner and reached apeak when Aβ1-42 came to 10 μmol/L; Compare with control group, the levels of TNF-α, IL-1β and NOincreased about 2 times, 13 times and 9 times, respectively. Exogenous CX3CL1 could decrease the levels ofTNF-α, IL-1β and NO in Aβ1-42-activated microglia cells by 45%, 24% and 38%, respectively. In conclusion,CX3CL1 could decrease the expression of inflammatory factors TNF-α, IL-1β and NO in Aβ1-42-activatedmicroglia cells, which indicates that CX3CL1 execute its neuroprotective functions by inhibiting the expression ofinflammatory factors.

关 键 词：小胶质细胞 CX3CL1 白介素-1Β 肿瘤坏死因子-Α 一氧化氮 

分 类 号：R749.16[医药卫生—神经病学与精神病学]