Oxidative stress is more likely to occur in the intestine compared to other organs because it is located at the interface between an organism and its luminal environment. Tannic acid (TA) is reported to serve as an antioxidant, antimicrobial, anticarcinogenic and antimutagenic agent in various models. In the present study, we evaluated the effects of TA on body weight, intestinal morphology, antioxidative activity, and intestinal barrier in diquat-induced oxidative stress mouse model. The results showed that TA had failed to affect antioxidative enzymes in diquat-challenged mice, while the concentration of 2.5 mg kg-1 to 10 mg kg-1 TA had no negative effect on body weight and enhanced the colon length in mice. The dose of 2.5 mg kg-1 TA ameliorated the morphological damage in the jejunum by increasing the villus height and crypt depth, activated the antioxidative pathway by decreasing jejunal protein expression of Kelch like-ECH-associated protein 1 (KEAP1) and increasing protein expression of Nuclear factor erythroid 2-related factor 2 (NRF2), and affected the intestinal barrier by inhibiting the jejunal mRNA expression of claudin and promoting mRNA expression of zonula occludens (zo-1). In conclusion, the pretreatment of TA in a mouse model of oxidative stress failed to change the antioxidative enzymes but modulated the jejunal morphology, colon length, antioxidative pathway and intestinal barrier in the diquat oxidative model.
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