Mir-30d increases intracellular survival of Helicobacter pylori through inhibition of autophagy pathway

Figure 1 Autophagy and mir-30d are upregulated in AGS and GES-1 cell lines in response to Helicobacter pylori infection. A: GFP-LC3 puncta were observed in AGS cells with or without 24 h Helicobacter pylori (H. pylori) infection. Quantification of the number of GFP-LC3 puncta in AGS and GES-1 cells presented as mean ± SD, ^aP < 0.05 control vs H. pylori infection; B: The autophagosomes and autophagolysosomes at 24 h after H. pylori infection assayed by transmission emission microscopy (TEM), shown are a typical autophagosome (black arrowheads) and autophagolysosome (white arrowheads). Quantification of GFP-LC3 puncta in AGS and GES-1 cells shown as mean ± SD, ^aP < 0.05 vs control; C: The protein levels of light chain (LC)3B-I and LC3B-II at 12 h and 24 h after infection with H. pylori analyzed by western blot; D: Analysis of the expression of mir-30d at 12 h and 24 h after infection with H. pylori in both cell lines by quantitative polymerase chain reaction (q-PCR). Results shown as mean ± SD, ^aP < 0.05 vs control.