Protective effect and mechanism of EGCG on intestinal inflammation and intestinal barrier function in mice induced by trinitrobenzenesulfonic acid

ObjectiveTo explore the effect and possible mechanism of epigallocatechin gallate (EGCG) on 2, 4, 6-trinitrobenzene sulfonic acid(TNBS)-induced colitis mice.

MethodsTwenty-four male C57BL/6J mice were randomly divided into model group (Model group), control group(WT group) and EGCG intervention group(EGCG group).The colitis was induced with TNBS in Model group and EGCG group.After the model was successfully made, the EGCG group was intraperitoneally injected with 15 mg·kg^-1·d^-1 EGCG, and the WT group and Model group were given the same amount of 0.9% sodium chloride solution.After 4 weeks of intervention, HE staining, immunofluorescence, Western blotting, bacteria culture and so on were used to analyze the intestinal inflammation, levels of intestinal mucosa inflammation mediators, intestinal barrier structure and function, and changes of JAK2/STAT3 signal in intestinal mucosa.

ResultsThe body mass gain of mice in EGCG group was higher than that in Model group(P < 0.05), and there was no significant difference compared with the WT group(P>0.05).At 3 to 4 weeks of intervention, the enteritis DAI score in EGCG group was significantly lower than that in Model group(P < 0.01).After 4 weeks of intervention, the intestinal inflammation scores, intestinal mucosa IL-6 and TNF-α levels of mice in EGCG group were lower than those in Model group(P < 0.05), but higher than those in WT group(P < 0.05);at the same time, the levels of intestinal epithelial tight junction proteins Occludin and ZO-1 were higher than those in Model group(P < 0.05), and there was no significant difference compared with the WT group(P>0.05).The results of in vivo permeability test showed that the serum FITC-dextran level in EGCG group was lower than that in Model group(P < 0.05), but higher than that in WT group(P < 0.05);while the proportion of bacterial translocation in liver and mesenteric lymph nodes was lower than that in Model group(P < 0.05), and there was no significant difference compared with the WT group(P>0.05).Western blotting analysis showed that the levels of p-JAK2 and p-STAT3 in the intestinal mucosa in EGCG group were lower than those in Model group(P < 0.05), and there was no significant difference compared with the WT group(P>0.05).

ConclusionsEGCG intervention in vivo can protect TNBS-induced Crohn's disease-like intestinal inflammation, which may be related to the protection of intestinal barrier function and inhibition of JAK2/STAT3 inflammation signal.