Baicalin inhibits autophagy induced by influenza A virus H3N2

• Influenza A virus A3/Beijing/30/95 (H3N2) induced autophagy by suppressing mTOR signaling pathway.
• We found that baicalin inhibited autophagy induced by influenza A virus H3N2.
• Baicalin could suppress the expression of Atg-5–Atg12 and LC3-II.
• Baicalin inhibited autophagy induced by starvation.
• Baicalin could alleviate mTOR upstream biochemical changes induced by virus infection.

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.