咖啡鞣酸抑制HSV-1感染的小胶质细胞系的炎性反应
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摘要
目的探究咖啡鞣酸(CGA)对单纯疱疹病毒(HSV)-1感染的小胶质细胞系BV2的抗炎作用。方法用HSV-1刺激BV2细胞建立单纯疱疹病毒性脑炎(HSE)的细胞模型,然后用不同浓度梯度的CGA进行处理;MTT法测定细胞存活率;实时定量PCR以及ELISA检测肿瘤坏死因子-α(TNF-α)和白介素(IL)-6含量及表达。结果 CGA处理后细胞存活率显著改善,在HSV-1感染BV2细胞后,CGA抑制了显著增高的TNF-α和IL-6的mRNA水平。此外,CGA减少HSV诱导的TNF-α和IL-6在细胞上清液中的释放(P<0.05)。结论 CGA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 investigate the anti-inflammatory effect of chlorogenic acid( CGA) on BV2 microglia infected by herpes simplex virus( HSV)-1. Methods BV2 cell was stimulated by HSV-1 to create a cell model of virus encephalitis,then CGA was processed with different concentrations. MTT method was used to measure cell viability. Real-time quantitative PCR and ELISA were used to detect the content and expression of tumor necrosis factor alpha( TNF-alpha) and interleukin( IL)-6. Results After CGA treatment,the cell survival rate significantly improved,and after HSV-1 infected BV2 cells,CGA inhibited the significant increase in mRNA levels of TNF-alpha and IL-6. In addition,CGA can reduce the release of TNF-alpha and IL-6 induced by HSV in the cells. The mRNAs of TNF-alpha and IL-6 were also significantly inhibited by CGA.Conclusions CGA inhibits inflammatory response in HSE.CGA can be used as an anti-inflammatory agent to treat HSE new strategies.
Objective To investigate the anti-inflammatory effect of chlorogenic acid( CGA) on BV2 microglia infected by herpes simplex virus( HSV)-1. Methods BV2 cell was stimulated by HSV-1 to create a cell model of virus encephalitis,then CGA was processed with different concentrations. MTT method was used to measure cell viability. Real-time quantitative PCR and ELISA were used to detect the content and expression of tumor necrosis factor alpha( TNF-alpha) and interleukin( IL)-6. Results After CGA treatment,the cell survival rate significantly improved,and after HSV-1 infected BV2 cells,CGA inhibited the significant increase in mRNA levels of TNF-alpha and IL-6. In addition,CGA can reduce the release of TNF-alpha and IL-6 induced by HSV in the cells. The mRNAs of TNF-alpha and IL-6 were also significantly inhibited by CGA.Conclusions CGA inhibits inflammatory response in HSE.CGA can be used as an anti-inflammatory agent to treat HSE new strategies.
引文
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[4]Gill N,Deacon PM,Lichty B,et al.Induction of innate immunity against herpes simplex virus type 2 infection via local delivery of Toll-like receptor ligands correlates with beta interferon production[J].J Virol,2006,80:9943-9950.
[5]Wang X,Li Y,Liu S,et al.Direct activation of RIP3/MLKL-dependent necrosis by herpes simplex virus 1(HSV-1)protein ICP6 triggers host antiviral defense[J].Proc Natl Acad Sci U S A,2014,28,111:15438-15443.
[6]Shen W,Qi R,Zhang J,et al.Chlorogenic acid inhibits LPS-induced microglial activation and improves survival of dopaminergic neurons[J].Brain Res,2012,88:487-494.
[7]Huang Y,Chen H,Zhou X,et al.Inhibition effects of chlorogenic acid on benign prostatic hyperplasia in mice.Eur[J].Pharmacol,2017,14.
[8]Royer DJ,Zheng M,Conrady CD,et al.Granulocytes in ocular HSV-1 infection:opposing roles of mast cells and neutrophils[J].Invest Ophthalmol Vis Sci,2015,56:3763-3775.
[9]Hu Y,Liu JP,Zhu Y,et al.The importance of toll-like receptors in NF-κB signaling pathway activation by helicobacter pylori infection and the regulators of this response[J].Helicobacter,2016,21:428-440.
[10]Villalba M,Hott M,Martin C,et al.Herpes simplex virus type 1 induces simultaneous activation of Toll-like receptors 2 and 4 and expression of the endogenous ligand serum amyloid A in astrocytes[J].Microbiol Immunol,2012,201:371-379.
[11]Guo YJ,Luo T,Wu F,et al.Involvement of TLR2 and TLR9 in the anti-inflammatory effects of chlorogenic acid in HSV-1-infected microglia[J].Life Sci,2015,127:12-18.
[12]Cai M,Li M,Wang K,et al.The herpes simplex virus 1-encoded envelope glycoprotein B activates NF-κB through the Toll-like receptor 2 and My D88/TRAF6-dependent signaling pathway[J].PLo S One,2013,8:e54586.doi:10.1371/journal.pone.0054586.
[13]Leoni V,Gianni T,Salvioli S,et al.Herpes simplex virus glycoproteins g H/g L and g B bind Toll-like receptor 2,and soluble g H/g L is sufficient to activate NF-κB[J].J Virol,2012,86:6555-6562.