Fig. 6 | Scientific Reports

Fig. 6

From: Helicobacter pylori CagA mediated mitophagy to attenuate the NLRP3 inflammasome activation and enhance the survival of infected cells

Fig. 6

Inhibition of Mitophagy can increase NLRP3 inflammasome activation of H. pylori infected cells. AGS and GES-1 cells were pretreated with mitophagy inhibitor (BafA1, 10 μM) for 24 h, respectively, and then infected with GZ7/cagA and GZ7/Δ cagA at an MOI of 60 for 48 h, respectively. (A) Western blotting analysis of the effect of BafA1treatment on the expression of mitophagy-related protein P62 and PARKIN in AGS and GES-1 cells. (B) Western blotting analysis of the effect of BafA1 treatment on the expression of NLRP3 inflammasome protein NLRP3, Caspase-1 and IL-18 in AGS and GES-1 cells. (C) Western blotting analysis of the effect of BafA1 pretreatment on the expression of NLRP3 inflammasome protein NLRP3, Caspase-1 and IL-18 in AGS and GES-1 cells with H. pylori infection. The figure presents the average of three independent experiments. Data are presented as the means ± SD. Error bars represent the standard deviation. control, the uninfected cells; GZ7/ΔcagA, the GZ7/ΔcagA strains infected cells; GZ7/cagA, the GZ7/cagA strains infected cells; *p < 0.05, **p < 0.01; GZ7/cagA vs control, GZ7/cagA vs BafA1 + GZ7/cagA, BafA1 + GZ7/cagA vs BafA1 + GZ7/ΔcagA.

Back to article page