Fig. 1From: Autophagy is involved in the replication of H9N2 influenza virus via the regulation of oxidative stress in alveolar epithelial cellsAutophagy is involved in H9N2 influenza virus replication (I). A549 cells were pre-treated with 10 μM LY294002, 10 mM 3-MA for 2 h, followed by infection with the H9N2 influenza virus (MOI = 1). (a, b) Cells were collected at 24 h p.i. and the protein expression levels of LC3-II were detected by western blot analysis. The expression levels of LC3-II were examined as ratios of intensities of GAPDH bands. **P < 0.01 relative to control. ##P < 0.01 relative to H9N2. (c) Fluorescence of GFP-LC3B was analyzed by confocal microscopy at 24 h p.i.. a: Control cells. b: H9N2 treated cells. c: H9N2 and LY294002 treated cells. d: H9N2 and 3-MA treated cells. (d–f) A549 cells were pre-treated with 100 nM rapamycin for 12 h, 10 μM LY294002, 10 mM 3-MA for 2 h, followed by infection with the H9N2 influenza virus. Supernatants from A549 cells were collected, and the viral titer was determined by measuring TCID50;**P < 0.01 relative to H9N2Back to article page