清透邪热方对甲型H1N1流感病毒感染Ana-1细胞TLR-7、MyD88及NF-κB mRNA及蛋白表达的影响

Effects of Qingtouxiere Decoction on Expression of TLR-7， MyD88 and NF-κB mRNA and Protein in Ana-1 Cells of Influenza A H1N1 Influenza Virus

    摘要
  • 摘要: 目的 研究清透邪热方体外抗甲型H1N1流感病毒效应机制。方法 将清透邪热方制备成0.388、0.194、0.097、0.0485、0.02425mg/mL不同浓度，用H1N1甲型流感病毒感染小鼠Ana-1巨噬细胞，给予不同浓度清透邪热方及达菲进行干预，检测肿瘤坏死因子α（TNF-α）、干扰素诱导蛋白-10（IP-10）和白细胞介素-6（IL-6）表达，Toll样受体7（TLR7）及其下游髓样分化因子88(MyD88)、核因子-κB（NF-κB）mRNA和蛋白表达。结果 清透邪热方能够抑制甲型H1N1流感病毒感染Ana-1细胞TNF-α、IP-10、IL-6的表达；其中清透邪热方0.02425mg/mL组降低H1N1病毒感染组TNF-α、IL-6显著（P＜0.01）；清透邪热方0.097mg/mL组降低IP-10显著（P＜0.01）。清透邪热方能够抑制H1N1流感病毒感染后Ana-1细胞后TLR-7、MyD88及NF-κB mRNA及蛋白表达升高；其中清透邪热方0.0485mg/mL组抑制H1N1病毒感染组TLR-7 mRNA、MyD88 mRNA表达显著（P＜0.01）；清透邪热方0.02425mg/mL组抑制H1N1病毒感染组NF-κB mRNA表达显著（P＜0.01）；清透邪热方0.0485mg/mL组抑制H1N1病毒感染组TLR-7蛋白表达升高显著（P＜0.01），清透邪热方0.388mg/mL组抑制H1N1病毒感染组MyD88蛋白、NF-κB蛋白表达显著（P＜0.01）。结论 清透邪热方通过抑制甲型H1N1流感病毒感染Ana-1细胞TLR-7、MyD88及NF-κB mRNA及蛋白表达升高，减少TNF-α、IP-10和IL-6表达，起到抗病毒作用。

     

    Abstract: OBJECTIVE To observe the effect mechanism of Qingtouxiere Decoction on anti-influenza A H1N1 influenza virus in vitro. METHODS The macrophages were stimulated with FM1 in the lungs of influenza A virus， respectively， with different concentrations of 0.388mg/mL， 0.194mg/mL， 0.097mg/mL， 0.0485mg/mL and 0.02425mg/mL. The expression of TNF-α， IP-10 and IL-6， TLR-7， mRNA and protein expression of MyD88 and NF-κB. RESULTS The expression of TNF-α， IP-10 and IL-6 in macrophages of Ana-1 mice was inhibited by Qingtouxiere Decoction， and the infection of H1N1 virus was decreased in 0.02425mg/mL group (P<0.01). The level of TNF-α was significantly lower in the group of Qingtouxiere Decoction 0.097mg/mL (P <0.01). The expression of TLR-7， MyD88 and NF-κB mRNA and protein were increased after Ana-1 macrophage infection in H1N1 influenza virus group. The expression of TLR-7， MyD88 and NF-κB mRNA was increased by 0.0485mg/mL group (P<0.01). The expression of MyD88 mRNA in the H1N1 infected group was significantly higher than that in the control group (P <0.01). The expression of TLR-7 mRNA was significantly inhibited The expression of NF-κB mRNA in H1N1 virus group was significantly higher than that in H1N1 virus group (P<0.01). The expression of TLR-7 protein in H1N1 virus group was significantly higher than that in H1N1 virus group(P<0.01). The expression of NF-κB in the H1N1 infected group was significantly higher than that in the H1N1 virus group (P<0.01). The expression of NF-κB in the H1N1 infected group was significantly higher than that in the control group (P<0.01). CONCLUSION The activation of TLR-7/MyD88/NF-κB signaling pathway induced by H1N1 influenza virus can inhibit the expression of downstream inflammatory factors and play the antiviral effect.

     

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