FENGLi-qian, YANGLi-li, LIMing-zhen, SUNYu, LIUTao. 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[J]. Journal of Nanjing University of traditional Chinese Medicine, 2017, 33(3): 289-294.
Citation: FENGLi-qian, YANGLi-li, LIMing-zhen, SUNYu, LIUTao. 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[J]. Journal of Nanjing University of traditional Chinese Medicine, 2017, 33(3): 289-294.

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

  • 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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