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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 expression of NF-κB signaling pathway-related factors and the regulation of baicalin and luteolin-7-O-glucoside induced by influenza virus H1N1 in vitro. Methods: Normal cells were inoculated with 100TCID50 virus solution. After adsorption for 2h, baicalin (3.96,0.99mg / L) and luteolin (25.0,12.5mg / L) ) As a positive control. Gene chips were used to analyze the differentially expressed inflammatory cytokines in each group. The mRNA and protein expression of NF-κB signaling pathway were detected by RT-PCR and Western blot. Results: Compared with normal control group, the expression of IRAK1, RIPK1, TAB2, NFKB, IL1B, IL8, TNFA and COX-2 were significantly up-regulated in H1N1 infection group. Compared with H1N1 infection group, IL1B and TNFA were significantly down-regulated and NFKBIA was significantly up-regulated. The expressions of IRAK1, RIPK1, TAB2, NFKB, IL1B, IL8 and TNFA in high and low doses of baicalin were significantly down-regulated and NFKBIA and TNFAIP3 were up- The genes RIPK1, IRAK1, TAB2, NFKB, IL1B, TNFA and COX-2 were significantly down-regulated and up-regulated NFKBIA. CONCLUSION: Influenza virus can activate NF-κB signaling pathway and cause over-expression of inflammatory cytokines. Baicalin and luteolin can regulate the positive and negative feedback of activation pathway and reduce the inflammatory damage of host cells, Virus effect.