Tannic acid alleviates ETEC K88‐induced intestinal damage through regulating the p62‐keap1‐Nrf2 and TLR4‐NF‐κB‐NLRP3 pathway in IPEC‐J2 cells

Abstract

BackgroundTannic acid (TA), a naturally occurring polyphenol, has shown diverse potential in preventing intestinal damage in piglet diarrhea induced by ETEC K88. However, the protective effect of TA on ETEC k88 infection‐induced post‐weaning diarrhea and its potential mechanism has not been well elucidated. Therefore, an animal trial was carried out to investigate the effects of dietary supplementation with TA on the intestinal diarrhea of weaned piglets challenged with ETEC K88. In addition, porcine intestinal epithelial cells were used as an in vitro model to explore the mechanism through which TA alleviates intestinal oxidative damage and inflammation.ResultsThe results indicated that TA supplementation (2 g·kg‐1 and 4 g·kg‐1) reduced diarrhea rate, enzyme activity (DAO and MAD) and serum inflammatory cytokines concentration (TNF‐α, IL‐1β) (P < 0.05) compared to the IG group in vivo. In vitro, TA treatment effectively alleviated ETEC‐induced cytotoxicity, increased the expression of ZO‐1, occludin and claudin‐1 at both mRNA and protein levels. Moreover, TA pre‐treatment increased the activity of antioxidant enzymes (such as T‐SOD) and decreased serum cytokine levels (TNF‐α, IL‐1β). Furthermore, TA increased cellular antioxidant capacity by activating the Nrf2 signaling pathway and decreased inflammatory response by down‐regulating the expression of TLR4, MyD88, NF‐kB and NLRP3.ConclusionThe study showed that TA reduced the diarrhea rate of weaned piglets by restoring the intestinal mucosal mechanical barrier function, alleviating oxidative stress and inflammation. The underlying mechanismwas achieved by modulating p62‐keap1‐Nrf2 and TLR4‐NF‐κB‐NLRP3 pathway.This article is protected by copyright. All rights reserved.