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作 者:刘晓婷[1] 顾立刚[1] 邓东沅 于卓男[1] 王玥琦[1] 吴珺[1] 邱泽计[1]
出 处:《中华中医药杂志》2016年第5期1937-1941,共5页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:国家自然科学基金资助项目(No.81173371)~~
摘 要:目的:探讨流感病毒H1N1体外感染诱导细胞NF-κB信号通路相关因子表达及黄芩苷和木犀草素-7-O-葡萄糖苷的调控作用。方法:正常生长细胞接种100TCID50的病毒液;吸附2h后分别加入黄芩苷(3.96、0.99mg/L)、木犀草苷(25.0、12.5mg/L),并以奥司他韦(0.75mg/L)做阳性对照。采用基因芯片技术分析各组细胞差异表达炎性因子。以RT-PCR和Western blot法检测细胞NF-κB信号通路相关因子m RNA和蛋白的表达变化。结果:与正常细胞对照组比较,H1N1感染组差异表达基因IRAK1、RIPK1、TAB2、NFKB、IL1B、IL8、TNFA和COX-2明显上调;与H1N1感染组比较,奥司他韦对照组基因NFKB、IL1B和TNFA明显下调,NFKBIA明显上调;黄芩苷高、低剂量组基因IRAK1、RIPK1、TAB2、NFKB、IL1B、IL8和TNFA明显下调,NFKBIA和TNFAIP3上调;木犀草苷高、低剂量组对差异表达基因RIPK1、IRAK1、TAB2、NFKB、IL1B、TNFA和COX-2明显下调,对NFKBIA上调作用。结论:流感病毒感染后活化NF-κB信号通路,引起炎性因子过度表达;黄芩苷和木犀草苷可以对活化通路的正负反馈进行调节,减轻病毒对宿主细胞的炎性损伤作用,发挥抗病毒作用。Objective: To investigate the regulatory effects and mechanism of baicalin and luteolin-7-O-glucoside on NF-κB signaling pathway induced by influenza virus H1N1 in human pulmonary carcinoma cell line A549. Methods: The normal A549 cells were infected with 100TCID50 influenza virus H1N1. After 2 hours, baicalin(3.96, 0.99mg/L), luteolin-7-Oglucoside(25.0, 12.5mg/L) and oseltamivir(0.75mg/L) were used to treat the cells. Some differential genes involved in NF-κB signal pathway were selected by DNA microarray, the candidate genes were verified by real-time PCR and Western blot. Results: Compared with normal group, IRAK1, RIPK1, TAB2, NFKB, IL1 B, IL8, TNFA and COX-2 were significant up-regulation in the virus-infected group. Compared with virus-infected group, NFKB, IL1 B and TNFA were down-regulated and NFKBIA up-regulated in oseltamivir group. IRAK1, RIPK1, TAB2, NFKB, IL1 B, IL8 and TNFA were down-regulated, NFKBIA and TNFAIP3 up-regulated in baicalin group. RIPK1, IRAK1, TAB2, NFKB, IL1 B, TNFA and COX-2 were down-regulated and NFKBIA were up-regulated in luteolin-7-O-glucoside groups. Conclusion: Baicalin and luteolin-7-O-glucoside could regulate the over-expression genes in NF-κB signaling pathway caused by influenza virus H1N1 infection, thus reducing inflammation and restoring stability and balance of body's immune function in vitro.
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