Baicalin inhibits autophagy induced by influenza A virus H3N2

Antiviral Res. 2015 Jan:113:62-70. doi: 10.1016/j.antiviral.2014.11.003. Epub 2014 Nov 10.

Abstract

Baicalin, a natural product isolated from Scutellariaradix, has been reported to have significant in vivo and in vitro anti-influenza virus activity, but the underlying mechanism remains poorly understood. In this study, we found that baicalin inhibited autophagy induced by influenza virus A3/Beijing/30/95 (H3N2) in both A549 and Ana-1 cells. The results showed that H3N2 induced autophagy by suppressing mTOR signaling pathway, which however could be significantly inhibited by baicalin. Baicalin could suppress the expression of Atg5-Atg12 complex and LC3-II, and attenuate autophagy induced by starvation. Thus, the inhibition of autophagy induced by virus may account for the antiviral activities of baicalin against H3N2. Autophagy may be a potential marker in developing novel anti-influenza drugs.

Keywords: Autophagy; Baicalin; H3N2; Influenza A virus.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antiviral Agents / pharmacology*
  • Autophagy / drug effects*
  • Cell Line
  • Cell Line, Tumor
  • Dogs
  • Flavonoids / pharmacology*
  • Flavonoids / toxicity
  • Humans
  • Influenza A Virus, H3N2 Subtype / physiology*
  • Macrophages / virology
  • Madin Darby Canine Kidney Cells
  • Mice
  • Real-Time Polymerase Chain Reaction
  • Scutellaria
  • Signal Transduction / drug effects
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Antiviral Agents
  • Flavonoids
  • baicalin
  • TOR Serine-Threonine Kinases