The Signal Pathways of Immune Inflammation Mediated by the Tlr3/Nf-Kappab and Activator Protein-1 in Cells Infected with Influenza A Virus Antagonized by Baicalin

Abstract

Baicalin has better anti-inflammatory function, antioxidant function and antiviral activity, but the mechanism of the antiinfluenza viral activity of baicalin has not been revealed.Toll-like Receptor 3 and the signal pathways mediated by TLR3 were affected and controlled by the infections with influenza A virus. We report here the significant activity and part mechanism of baicalin against H3N2 influenza A viruses. Baicalin could well protect the damages of cells caused by influenza A virus, it also could effectively inhibit the production of CPE in cells caused by influenza A virus and the inhibition of cells growth. The mechanism of antiinfluenza virus infection of baicalin may be related with the following aspects: to decrease the transcriptional activity of the oxidative stress sensitive transcription factor NF-kappaB and AP-1 by moderately decrease the higher expression level of TLR3 mRNA and the higher expression level of protein; and to further inhibit the mRNA expression of the downstream target genes IL-1β, IL-8, RANTES and IFN-β thereby alleviate the inflammatory injuries and restore the stability and balance of immune function in vivro.