Gallic acid alleviates colitis by restoring intestinal barrier function and enriching butyrate-producing bacteria.

Abstract

Ulcerative colitis (UC), a chronic inflammatory bowel disease, exhibits increasing global prevalence. However, there remains a paucity of evidence on whether gallic acid (GA) can be used to mitigate acute and chronic colitis. In this study, the underlying mechanism of GA in alleviating UC was thoroughly investigated. Our results showed that GA protected mice from acute and chronic colitis, evidenced by relieved pathological symptoms of UC, strengthened the tight junction, and repaired the damaged intestinal barrier. Moreover, GA regulated the balance of microbiota in the gut and increased the abundance of beneficial bacteria, especially probiotics and butyric acid-producing bacteria, such as Lachnospiraceae NK4A136. Finally, we established a co-culture model of Caco-2/RAW264.7 cells mimicking the gut barrier, GA and butyrate reduced inflammation and repaired barrier function in LPS-induced inflammation. Notably, the combined treatment of GA and butyrate showed more significant alleviation of LPS-induced inflammation and intestinal barrier damage. These findings indicated that GA effectively alleviates colitis in mice, and this effect was associated with restored intestinal barrier integrity and increased abundance of butyrate-producing bacteria. This work provides a foundation for considering GA as a potential therapeutic candidate for UC.