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机构地区:[1]湖北职业技术学院医学院,孝感432000 [2]华中科技大学同济医学院附属同济医院,武汉430030
出 处:《国际免疫学杂志》2014年第1期64-68,共5页International Journal of Immunology
基 金:国家青年基金项目(NSFC81100262);中国博士后科学基金项目(2013M531700)
摘 要:目的在脂多糖(LPS)激活的小胶质细胞(MG)基础上观察姜黄素(Cur)对BV2细胞合成单核细胞趋化因子(MCP-1)的影响,并探讨其可能的分子机制。方法采用酶联免疫吸附、实时定量PCR技术检测Cur对BV2细胞合成趋化因子MCP-1的影响,通过Western blot观察NF—κB活化和细胞外调节蛋白激酶(ERK)磷酸化进一步探讨其分子机制。结果与LPS刺激的细胞相比较,Cur能够明显降低MCP-1、TNF-α和IL-1β基因水平和蛋白水平表达(F值分别为70.95、52.91和40.18,P〈0.05或P〈0.01),其抑制效应随着Cur浓度增加而更加显著;Cur处理明显抑制NF—κB(p65)核移位(F值为31.50,P〈0.05)并降低ERK磷酸化水平(F值为36.66,P〈0.05),该阻断作用随着Cur浓度增加而愈加显著。结论Cur对能抑制LPS激活的小胶质细胞的趋化能力,其分子机制与抑制NF—κB核移位和ERK磷酸化有关。Objective To investigate the effects of Curcumin(Cur) on chemotaxis of lipopolysaccharides(LPS) -stimulated BV2 microglia. Methods BV2 cells were treated by Cur at different concentrations in the presence or absence of LPS. Changes of monocyte chemoattractant protein-1 ( MCP-1 ), tumor nectosis factor-alpha (TNF-α) and interleukin-lbeta (IL-1 β) were detected by enzyme-linked immunosorbent assay and Real-time quantitative PCR technique. Nuclear factor-kappa B (NF-κB)p65 translocation and extracellular regulated protein kinases(ERK) phosphorylation were assayed by Western blot technique. Results The MCP-1, TNF-α and IL-1β were inhibited by Cur at both protein and mRNA levels significantly. Moreover, NF-κB p65 activation and ERK phosphorylation were suppressed by Cur marketly. With the increasing concentration of Cur,the inhibiting effect of Cur becames more and more intense. Conclusions Cur can inhibited the MCP-1 production in LPS-stimulated BV2 microglias through down-regulating NF-κB activation and ERK1/2 phosphorylation.
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