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作 者:邓娜 赵雷[2] DENG Na;ZHAO Lei(Children's Medical Center, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000;Department of Infection Disease, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan , Hubei 430000, China)
机构地区:[1]湖北医药学院附属人民医院儿童医疗中心,湖北十堰442000 [2]华中科技大学同济医学院附属协和医院感染科,湖北武汉430000
出 处:《湖北医药学院学报》2018年第1期24-28,34,F0003,共7页Journal of Hubei University of Medicine
基 金:国家自然科学基金(81371840)
摘 要: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.
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