Antagonism of geniposide on Toll-like receptor 7/nuclear factor-κB signaling pathways in cells with influenza A virus infection
10.3760/cma.j.issn.0254-5101.2010.08.014
- VernacularTitle:栀子苷抑制甲型流感病毒感染细胞中Toll样受体7/核因子-κB信号通路
- Author:
Chunjing ZHANG
;
Haitao YU
- Publication Type:Journal Article
- Keywords:
Geniposide;
Type A influenza virus H3N2;
Toll-like receptor 7/nuclear factor-κB signaling pathways;
Inflammatory cytokines
- From:
Chinese Journal of Microbiology and Immunology
2010;30(8):749-754
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe how geniposide as an anti-inflammatory agent through inhibition Toll-like receptor 7/nuclear factor-κB signaling pathways activation, as well as TNF-α and IL-6 release infectioned by influenza virus. Methods Epithelial cells was exposed to human influenza viruses A/Gui/81/23(H3N2) infection for 2 h before treatment with geniposide for 24 h. NF-κB responsive element luciferase reportor gene was transfected and dual luciferase cis-reporting systems was used to assay the transcriptional activity of NF-κB under the stimulated circumstance of influenza virus infection. The phosphory level and nuclear transposition of NF-κB was observed by fluorescence inverted microscope. RT-PCR was used to detect the gene transcription level of TLR7, TNF-α and IL-6. Results The relative luciferase reporter assay of NF-κB was apparently improved by influenza virus infection. But geniposide significantly repressed the relative value of luciferase. The phosphorylation level and rate for nuclear transposition of NF-κB was apparently improved by influenza A virus infection observed by fluorescence inverted microscope. But geniposide significantly repressed the phosphorylation level and rate for nuclear transposition. RT-PCR showed upregulation of TLR7 and pre-inflammatory markers TNF-α and IL-6 in A549 cells infected by influenza virus, geniposide had a significant effect on the expression of TLR7 and inflammatory markers TNF-α and IL-6 after treated with influenza virus. Conclusion Geniposide as an antiinflammatory agent antagonized influenza A virus infection through inhibiting Toll-like receptor 7/nuclear factor-κB signaling pathways activation, as well as on the downregulation of the downstream inflammatory markers target gene expression TNF-α and IL-6.
