咖啡鞣酸在HSV-1感染的小胶质细胞中通过TLR2通路的抗炎机制研究

Involvement of TLR2 in the Anti-inflammatory Effects of Chlorogenic acid in HSV-1-infected Microglia

目的:探讨咖啡鞣酸(CGA)对单纯疱疹病毒(HSV)-1感染的BV2小胶质细胞的抗炎治疗效果。方法:用HSV-1刺激的BV2细胞建立单纯病毒脑炎的细胞模型,然后用不同浓度梯度的CGA进行处理。通过MTT法测定细胞存活率。通过real-time PCR测定Toll样受体(TLR)-2 mRNA表达,并通过流式细胞术或Western Blot测定蛋白质的表达。核因子NF-κB p65蛋白通过Western Blot测定。结果:CGA治疗后细胞存活率显著改善,在HSV-1感染后BV2细胞后,CGA阻止了在mRNA和蛋白质水平上TLR2的增加。NF-κBp65的表达在HSV-1刺激的小胶质细胞核中显著增加,但CGA作用后可减少。结论:CGA通过抑制TLR2信号通路的传导抑制HSE中的炎性反应。CGA可以作为一种抗炎剂提供治疗HSE的新策略。

Objective To explore the anti-inflammatory effect of chlorogenic acid（ CGA） on BV2 microglial cells infected with herpes simplex virus（ HSV）-1. Methods The cell model of pure viral encephalitis was established using BV2 cells stimulated by hsv-1 and treated with CGA with different concentrations. Cell survival was measured by MTT method. The expression of toll-like receptor（ TLR）-2 mRNA was determined by real-time PCR,and protein expression was measured by flow cytometry or Western Blot. NF-kappa B p65 protein was determined by Western Blot. Results After CGA treatment,cell survival rate significantly improved,and in BV2 HSV 1 cells after infection,CGA blocked the increase of TLR2 at the mRNA and protein levels. The expression of NF-kappa Bp65 significantly increased in the microglia nucleus of hsv-1,but decreased after CGA treatment. Conclusion CGA inhibits the inflammatory response in HSE by inhibiting the conduction of TLR2 signaling pathway. CGA can be used as an anti-inflammatory agent to provide a new strategy for the treatment of HSE.