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作 者:吴小梅[1] 贾汝汝 张蕊 陈蕾[1] 朱俐[1] WU Xiaomei;JIA Ruru;ZHANG Rui;CHEN Lei;ZHU Li(Institute of Special Environmental Medicine,Nantong University,Jiangsu 226019)
出 处:《交通医学》2020年第6期570-572,共3页Medical Journal of Communications
基 金:国家自然科学基金项目(81971131)。
摘 要:目的:探讨趋化因子CX3CL1对小鼠小胶质细胞铁吸收的影响。方法:用6-羟基多巴胺(6-OHDA)或柠檬酸铁铵(FAC)处理多巴胺能神经元细胞系MES23.5细胞,通过ELISA法检测MES23.5细胞趋化因子CX3CL1的释放;用CX3CL1和含CX3CL1的MES23.5条件培养基直接处理小鼠小胶质细胞系BV2细胞,或预先干扰CX3CL1受体CX3CR1后再行处理,采用钙黄绿素指示剂(Calcein-AM)观察BV2细胞对二价铁离子的吸收变化。结果:6-OHDA和FAC促进MES23.5细胞CX3CL1的释放,外源和内源性CX3CL1都可诱导BV2细胞对二价铁的吸收,这种诱导作用可被CX3CR1干扰阻断。结论:多巴胺能神经元释放的趋化因子CX3CL1可通过CX3CR1促进小胶质细胞对铁的吸收。Objective:To investigate the effect of fractalkine(CX3CL1)on iron uptake of microglia in mice.Method:Dopaminergic MES23.5 cells were treated with 6-hydroxydopamine(6-OHDA)or ferric ammonium citrate(FAC)for 12 h.After another 24 h culture,the content of CX3CL1 in supernatant medium of MES23.5 cells was measured by ELISA.The ferrous uptake of microglial BV2 cells was detected by using Calcein-AM indicator on divalent metal ions after they were treated directly with CX3CL1 or conditioned medium containing CX3CL1 from MES23.5 cells,and pre-treated with lentivirus encoded CX3CR1 shRNA before then.Results:6-OHDA and FAC promoted the release of CX3CL1 from MES23.5 cells into medium.Both exogenous and endogenous CX3CL1 induced the ferrous uptake of BV2 cells,but could be inhibited by CX3CR1 shRNA.Conclusion:CX3CL1 secreted from dopaminergic neurons could facilitate the ferrous uptake of microglia,which was mediated by its receptor CX3CR1.
关 键 词:CX3CL1 CX3CR1 小胶质细胞 铁 帕金森病
分 类 号:R742.5[医药卫生—神经病学与精神病学]
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