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通过观察TLR2蛋白阻断前后HCV阳性血清处理BV-2细胞培养上清液中MCP-1、IL-6及IL-12的表达,为进一步探讨HCV引起中枢神经系统免疫反应特点奠定基础。细胞分为空白对照组(常规培养用DMEM高糖培养液)、正常对照组(含有20%正常血清的DMEM高糖培养液)、实验组(含有20%HCV阳性血清的DMEM高糖培养夜),每组分为4 h、8h、16 h及24 h,同时设24 h阻断组(加TLR2单克隆抗体孵育30 min后给予含有20%HCV阳性血清的DMEM高糖培养液培养24 h),采用ELISA方法检测各组各时间点培养上清液中MCP-1、IL-6及IL-12的表达水平,并使用SPSS13.0统计软件对结果进行统计分析,结果发现HCV阳性血清处理后MCP-1、IL-6及IL-12的表达显著增加,与空白对照及正常血清对照组比较具有统计学意义(P<0.05);TLR2蛋白阻断后MCP-1、IL-6及IL-12的表达明显下降,与实验组24 h比较具有统计学意义(P<0.05)。本研究发现,HCV阳性血清处理后TLR2介导的MCP-1、IL-6及IL-12的表达明显增加,TLR2可能通过激活下游大量炎性因子参与BV-2抗HCV免疫。
By observing the expression of MCP-1, IL-6 and IL-12 in culture supernatant of BV-2 cells treated with HCV positive serum before and after the blocking of TLR2 protein, we lay the foundation for further exploring the characteristics of HCV-induced central nervous system immune response. The cells were divided into blank control group (DMEM high glucose culture medium for routine culture), normal control group (DMEM high glucose culture medium containing 20% normal serum), experimental group (DMEM high glucose culture medium containing 20% HCV positive serum) , Each group was 4 h, 8 h, 16 h and 24 h, at the same time set 24 h block group (plus TLR2 monoclonal antibody incubated 30 min after given 20% HCV-positive serum DMEM high glucose culture medium for 24 h) The expression of MCP-1, IL-6 and IL-12 in culture supernatants was detected by ELISA at each time point. Statistical analysis was carried out using SPSS 13.0 statistical software. As a result, it was found that after HCV positive serum treatment The expression of MCP-1, IL-6 and IL-12 were significantly increased compared with the control group and the blank control group (P <0.05) 12 expression was significantly decreased compared with the experimental group 24 h was statistically significant (P <0.05). The present study found that the expression of MCP-1, IL-6 and IL-12 was significantly increased after treatment with HCV-positive serum. TLR2 may be involved in the anti-HCV immunity of BV-2 by activating a large number of downstream inflammatory cytokines.