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作 者:吴婷 刘琳 王可鑫 杜俊蓉[1] 龙方懿[1,2] WU Ting;LIU Lin;WANG Kexin;DU Junrong;LONG Fangyi(West China School of Pharmacy,Sichuan University,Chengdu,Sichuan,610041 P.R.China;Laboratory Medicine Center,Sichuan Provincial Maternity and Child Health Care Hospital,Chengdu,Sichuan,610045 P.R.China)
机构地区:[1]四川大学华西药学院,四川成都610041 [2]四川省妇幼保健院实验医学中心,四川成都610045
出 处:《华西药学杂志》2025年第2期153-157,共5页West China Journal of Pharmaceutical Sciences
摘 要:目的探讨自然杀伤细胞活化受体(NKG2D)在氧糖剥夺刺激的小鼠小胶质细胞BV2炎症反应中的作用及其分子机制。方法建立小鼠神经元细胞HT22氧糖剥夺(OGD)模型,造模14 h后,复氧复糖,分别收集正常条件培养上清和OGD培养上清(OGD-CM)刺激小鼠小胶质细胞BV2;同时,应用慢病毒感染介导的RNAi技术敲减BV2细胞NKG2D的表达,并采用qRT-PCR、Western blot、ELISA与免疫荧光等技术检测OGD-CM刺激下BV2细胞中NKG2D相关炎症通路与下游炎症因子的水平。结果OGD-CM可激活BV2细胞NKG2D/DAP10/NF-κB信号通路,促进下游炎症因子肿瘤坏死因子-α(TNF-α)、白细胞介素6(IL-6)的产生;但NKG2D敲减可减弱OGD-CM诱导的BV2细胞NKG2D/DAP10/NF-κB信号通路激活,抑制下游炎症因子TNF-α、IL-6的产生。结论NKG2D敲减可能通过抑制NKG2D/DAP10/NF-κB信号通路,抑制OGD诱导的BV2细胞炎症反应,初步表明NKG2D在缺血性脑卒中的潜在作用及机制。OBJECTIVE To explore the role of natural killer group 2 member D(NKG2D)in the oxygen-glucose deprivation(OGD)-induced inflammatory response in mouse microglial BV2 cells and its underlying molecular mechanisms.METHODS The OGD model of HT22 mouse hippocampal neurons was established by OGD treatment for 14 hours followed by oxygen and glucose recovery.Normal conditioned medium and OGD conditioned medium(OGD-CM)were collected to stimulate BV2 cells.Lentiviral vector-mediated RNA interference was used to knockdown NKG2D expression in BV2 cells.Quantitative real-time PCR,Western blot,enzyme-linked immunosorbent assay and immunofluorescence were used to measure the levels of NKG2D-related inflammatory pathways and downstream inflammatory factors in BV2 cells stimulated with OGDCM.RESULTS OGDCM activated the NKG2D/DAP10/NF-κB signaling pathway in BV2 cells to promote the production of downstream inflammatory factors,including TNF-αand IL-6.However,NKG2D knockdown could inhibit the activation of the NKG2D/DAP10/NF-κB signaling pathway in BV2 cells induced by OGD-CM and the production of downstream inflammatory factors,including TNF-αand IL-6.CONCLUSION NKG2D knockdown may inhibit inflammation in BV2 cells induced by OGD-CM via the NKG2D/DAP10/NF-κB signaling pathway,which preliminarily demonstrats the potential role and mechanism of NKG2D in ischemic stroke.
关 键 词:自然杀伤细胞活化受体 NKG2D/H60/DAP10轴 氧糖剥夺 小胶质细胞 炎症反应 缺血性脑卒中 BV2细胞 核因子-κB
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