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作 者:邓娜[1] 王金堂[1] DENG Na;WANG Jintang(Department of Pediatrics,the People’s Hospital of Shiyan City,Hubei Province,Shiyan 442000,China)
出 处:《医药导报》2018年第10期1170-1173,共4页Herald of Medicine
摘 要:目的研究咖啡鞣酸(CGA)对单纯疱疹病毒-1(HSV-1)感染BV2小胶质细胞诱导单纯疱疹病毒性脑炎(HSE)细胞模型过程中Toll样受体2(TLR2)信号通路的干预机制。方法将细胞分为正常对照组、模型对照组和CGA低、中、高浓度组(25,50和100 ng·m L-1)。用HSV-1刺激的BV2细胞建立HSE的细胞模型,然后用不同浓度梯度的CGA进行处理。分别通过RT-PCR和Western blotting测定TLR2、Myd88 mRNA和蛋白质的表达。通过ELISA以及实时PCR(RT-PCR)测定IL-6的表达。结果模型对照组TLR2、Myd88、IL-6水平显著高于正常对照组(P<0.05),咖啡鞣酸干预后,其水平显著低于模型对照组(P<0.05)。结论在HSV-1感染BV2小胶质细胞诱导HSE细胞模型中,咖啡鞣酸可以通过抑制TLR2信号通路中TLR2、Myd88分子的表达,从而抑制促炎因子IL-6的释放,减轻炎性反应。Objective To investigate interference of chlorogenic acid(CGA)on TLR2 signal pathway in herpes simplex virus(HSV)-1-induced responses in BV2 microglia.Methods The cellular model was established with BV2 cells stimulated by HSV-1 and then treated with CGA at different concentrations.The mRNA expression of Toll-like receptor(TLR)-2 and Myd88 was assayed by real-time quantitative PCR(RT-PCR),and the protein expression was assayed by Western blotting.IL-6 levels in the serum were tested by ELISA and RT-PCR.Results TLR2,Myd88 and IL-6 were significantly higher in the model control group than in the normal control group(P<0.05).After CGA treatment,TLR2,Myd88,IL-6 were significantly lower than those in the model control group(P<0.05).Conclusion In HSV-1 infected microglia cellular model,CGA inhibits the inflammatory reaction via suppressing TLR2,Myd88,IL-6 in TLR2 signal pathway and inhibiting IL-6 release.
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