Ellagic acid alleviates TNBS-induced intestinal barrier dysfunction by regulating mucin secretion and maintaining tight junction integrity in rats

Abstract

In the present study, the mechanism of ellagic acid (EA) in alleviated ulcerative colitis (UC) was investigated. Twenty-four SD rats were randomly distributed into three treatment groups: (1) control group, (2) UC group, and (3) UC + EA group. Samples were collected for analysis after a 15-day trial period. We found that EA mitigated the colitis symptoms in TNBS-treated rats. Besides, EA decreased the expression of cytokines by inhibiting NF-κB signalling. TNBS-induced reduction in tight junction proteins was restored by EA supplementation via regulating RhoA/ROCK/MLC signalling. Further, persistent colonic inflammation destroyed the activity of goblet cells by inhibiting the expression of KLF4 and TFF3. EA also enhanced the expression of MUC2, AGR2, ST6GAL1 and B3GNT6. In summary, our findings demonstrated that dietary supplementation with EA ameliorated TNBS-induced colitis by maintaining intestinal barrier function, which proves its potential role as a therapeutic agent in the attenuation of UC.

Keywords:

• Ulcerative colitis
• ellagic acid
• inflammation
• intestinal barrier
• mucins
• rat

Author contributions

Bo Peng conducted experiments, analysed data, and wrote the manuscript. Prof. Linyun Xue and Tian Zhong helped review and edit the manuscript. Qian Yu provided knowledge for the design. Bo Peng acquired the funding. All authors have read and agreed to the published version of the manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

All data generated are included in the article.

Additional information

Funding

This work was supported by the Project of the Science and Technology Department of Sichuan Province [YFS0393].