Fig. 4

5-Aza re-activated Bcl6b and inhibited inflammatory responses. (a) WT and Bcl6b^−/− mice were given Bap for gastric cancer induction during weeks 10–25 of treatment with or without the demethylation drug 5-Aza at a dose of 0.5 mg/kg for 15 consecutive weeks. (b) Representative images showing immunostaining and Western blotting of Bcl6b expression in Bap-induced gastric tumours (25 week) from Bcl6b^−/− mice and WT controls with or without 5-Aza treatment. Scale bar, 50 μm. (c) Representative images and quantification of CD3-immunopositive cells in Bap-induced gastric tumours (25 week) from Bcl6b^−/− mice and WT controls with or without 5-Aza treatment. Scale bar, 50 μm. (d) qRT-PCR revealed TNF-α, IL-1β and IL-8 mRNA levels from stomachs harbouring BaP-induced tumours (25 week) from Bcl6b^−/− mice and WT controls with or without 5-Aza treatment. (e) ELISA revealed serum protein levels of TNF-α and IL-1β in WT and Bcl6b^−/− mice after intragastric administration of BaP (25 week) with or without 5-Aza treatment. Data are presented as the mean ± SD; n = 5 per group. *P < 0.05; **P < 0.01; ***P < 0.001; NS, not significant; unpaired two-tailed Student’s t tests