title: Baicalin inhibits autophagy induced by influenza A virus H3N2.
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.
authors.affiliation: Department of Biosynthesis, School of Pharmacy, Fudan University, 826 Zhangheng Road, Shanghai, China.
authors.forename: Hai-yan
authors.initials: HY
authors.lastname: Zhu
authors.affiliation: Department of Biosynthesis, School of Pharmacy, Fudan University, 826 Zhangheng Road, Shanghai, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Han
authors.affiliation: Department of Biosynthesis, School of Pharmacy, Fudan University, 826 Zhangheng Road, Shanghai, China.
authors.forename: Xun-long
authors.initials: XL
authors.lastname: Shi
authors.affiliation: Department of Biosynthesis, School of Pharmacy, Fudan University, 826 Zhangheng Road, Shanghai, China.
authors.forename: Bao-long
authors.initials: BL
authors.lastname: Wang
authors.affiliation: Department of Biosynthesis, School of Pharmacy, Fudan University, 826 Zhangheng Road, Shanghai, China.
authors.forename: Hai
authors.initials: H
authors.lastname: Huang
authors.affiliation: Department of Biosynthesis, School of Pharmacy, Fudan University, 826 Zhangheng Road, Shanghai, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Pharmacognosy, School of Pharmacy, Fudan University, 826 Zhangheng Road, Shanghai, China.
authors.forename: Dao-feng
authors.initials: DF
authors.lastname: Chen
authors.affiliation: Department of Biosynthesis, School of Pharmacy, Fudan University, 826 Zhangheng Road, Shanghai, China.
authors.forename: Dian-wen
authors.initials: DW
authors.lastname: Ju
authors.affiliation: Department of Biosynthesis, School of Pharmacy, Fudan University, 826 Zhangheng Road, Shanghai, China. Electronic address: fmq@fudan.edu.cn.
authors.forename: Mei-qing
authors.initials: MQ
authors.lastname: Feng
mesh_terms: D000818:Animals; D000998:Antiviral Agents / Q000494:pharmacology*; D001343:Autophagy / Q000187:drug effects*; D002460:Cell Line; D045744:Cell Line, Tumor; D004285:Dogs; D005419:Flavonoids / Q000494:pharmacology* / Q000633:toxicity; D006801:Humans; D053122:Influenza A Virus, H3N2 Subtype / Q000502:physiology*; D008264:Macrophages / Q000821:virology; D061985:Madin Darby Canine Kidney Cells; D051379:Mice; D060888:Real-Time Polymerase Chain Reaction; D031363:Scutellaria; D015398:Signal Transduction / Q000187:drug effects; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: D000998:Antiviral Agents; D005419:Flavonoids; C038044:baicalin; D058570:TOR Serine-Threonine Kinases
keywords: Autophagy; Baicalin; H3N2; Influenza A virus