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通过观察小鼠小胶质细胞BV2(BV2细胞)在HCV阳性血清处理后Toll样受体4(TLR4)表达及肿瘤坏死因子α(TNF-α)分泌变化,初步探讨HCV导致中枢神经系统损害时的可能固有免疫应答机制。应用RT-qPCR方法观察BV2细胞用含20%HCV阳性血清的培养液处理后6 h、12 h、18 h、24 h TLR4 mRNA的相对表达,用ELISA方法检测细胞培养上清液中TNF-α的含量,同时设20%正常人血清组和空白对照组。结果HCV实验组BV2细胞TLR4 mRNA表达、TNF-α分泌高于同一时间点正常血清组及空白对照组(P<0.01),HCV实验组BV2细胞24 h内TLR4 mRNA表达和TNF-α分泌均呈增高趋势且存在明显正相关(r=0.858)。提示HCV阳性血清处理可引起体外培养的BV2细胞TLR4表达上调,从而通过信号转导通路导致炎性细胞因子TNF-α分泌增加。TLR 4可能介导参与了中枢神经系统抗HCV固有免疫应答过程。
By observing the changes of Toll-like receptor 4 (TLR4) expression and tumor necrosis factor-α (TNF-α) secretion of mouse microglia BV2 (BV2 cells) after treatment with HCV-positive serum, we explored the effects of HCV on central nervous system Possible innate immune response mechanism. RT-qPCR method was used to observe the relative expression of TLR4 mRNA at 6 h, 12 h, 18 h, 24 h after culture of BV2 cells with 20% HCV-positive serum. ELISA was used to detect the expression of TNF-α Content, set 20% normal human serum group and blank control group. Results The level of TLR4 mRNA and the secretion of TNF-α of BV2 cells in HCV experimental group were higher than those in normal serum group and blank control group (P <0.01). The BV2 cells in HCV group showed a significant increase in TLR4 mRNA and TNF-α secretion within 24 hours Increasing trend and there is a clear positive correlation (r = 0.858). These results suggest that HCV positive serum treatment can induce the up-regulation of TLR4 expression in BV2 cells cultured in vitro, which leads to the increase of TNF-αin inflammatory cytokines through signal transduction pathway. TLR4 may mediate the central nervous system anti-HCV innate immune response process.