Fig. 3From: Glycyrrhizin, an inhibitor of HMGB1 induces autolysosomal degradation function and inhibits Helicobacter pylori infectionActivation of autophagic flux by glycyrrhizin treatment (a, b) Cells were incubated with H. pylori SS1 strain (4 h) followed by glycyrrhizin GLZ (200 µM) exposure for 4 h. a Glycyrrhizin (GLZ) exposure to H. pylori-infected cells for 4 h was subjected to LAMP1 and LC3B double immunofluorescence. Confocal microscopy showed yellow puncta with co-localization of LC3B puncta (green) & LAMP1 (red). Change in the co-localization coefficient of each group was calculated. Scale bar: 2 μm. b AGS cells were transfected with a tandem mRFP-GFP tag (tfLC3B) plasmid & further infected with H. pylori SS1 strain (MOI 100) for 4 h and finally, glycyrrhizin (GLZ) (200 µM) treatment was done for 4 h. Confocal microscopy showed LC3B puncta formation in control (CON), H. pylori (HP) infected & H. pylori + glycyrrhizin (HP + GLZ) treated cells. The yellow puncta showed autophagosomes. The free red puncta are autolysosomes. Change in the co-localization coefficient of each group was calculated. Scale bar: 2 μm. Graph represented as mean ± SEM (n = 3); Significance was determined by Unpaired t-test; *p < 0.05, ***p < 0.001Back to article page