Fig. 6

Treatment with STAT3 or NF-κB inhibitors reduced inflammation in TFF1-KO mice gastric tissues. a Immunofluorescence staining of phospho-NF-κB-P65 (Green) and phospho-STAT3 (Y705) (Red) in the antropyloric region of the glandular stomach of the TFF1-KO mice infected with PMSS1 H. pylori and treated or not by intraperitoneal injection with BAY (5 mg/Kg). In control, un-infected TFF1-KO showed more p-NF-κB-P65 and p-STAT3 nuclear staining after H. pylori infection (arrowheads). However, after treatment with BAY, staining showed reduced nuclear STAT3 and NF-κB (arrows). 4’, 6’ Diamino-2-phenylindole (DAPI) (blue) was used as a nuclear counterstain, original magnification (× 1000). b RT-qPCR analysis showing mRNA expression of pro-inflammatory target genes (Il-6, Vegf-α, Il-17 and IL-23) in H. pylori-infected TFF1-KO mice (10–12 weeks of age) treated or not with BAY (5 mg/Kg) and compared to TFF1-KO uninfected mice. Results are graphed using box-and-whisker blots to depict the smallest value, lower quartile, median, upper quartile, and largest value. (●) Indicate the mean. c A schematic cartoon depicting the role of TFF1 in regulating the inflammation in gastric epithelial cell through inhibition of NF-κB-mediated activation of STAT3 in response to H. pylori