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.