Fig. 4

Autophagy affected protein level of COX-2 in AGS cells infected with H. pylori. A Western blotting and autophagic flux assay in AGS cells pretreated with rapamycin for 24 h (n = 4, mean ± SD, *P < 0.05). B Western blotting and autophagic flux assay in AGS cells pretreated with chloroquine for 6 h (n = 4, mean ± SD, *P < 0.05). C Western blotting and signal intensity of COX-2 protein levels in AGS cells enhanced autophagy with rapamycin infected with Hp-WT and Hp-ΔcagA (n = 4, mean ± SD, *P < 0.05). D Western blotting and signal intensity of COX-2 protein levels in AGS cells inhibited autophagy with rapamycin infected with Hp-WT and Hp-ΔcagA (n = 4, mean ± SD, *P < 0.05). E Western blotting and autophagic flux assay in AGS cells transfected with BECN1 small interfering-RNA (n = 4, mean ± SD, *P < 0.05). F Western blotting and signal intensity of COX-2 protein levels in BECN1 knock down AGS cells infected with Hp-WT and Hp-ΔcagA (n = 5, mean ± SD, *P < 0.05). Hp-WT, wild-type cagA-positive H. pylori; Hp-ΔcagA, cagA-knockout H. pylori; CagA, cytotoxin-associated gene A; COX-2, cyclooxygenase 2