Tannic acid is a gastroprotective that regulates inflammation and oxidative stress.

This study investigated the gastroprotective effect of TA against gastric ulcer in mice, and its possible mechanisms of action. The effects were investigated in a model of ethanol and ethanol/HCl induced ulcers, and physical barrier test. Quantification of oxidative stress mediators and inflammatory cytokines in gastric tissue was performed. The involvement of sulfhydryl compounds (-SH), nitric oxide (NO), prostaglandin E (PGE), potassium channels (K ) and opioid receptors in gastroprotection were investigated. Oral treatment with TA at a dose of 50 mg/kg resulted in 97.96% and 94.20% (reduction in gastric injury) of gastroprotection, against injuries caused by ethanol and ethanol/HCL, respectively, in addition to having a systematic effect. TA promotes increased levels of superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH), as well as reduced levels of malondialdehyde (MDA) reaction to thiobarbituric acid and myeloperoxidase (MPO). In addition, there was reduction in levels of tumor necrosis factor alpha (TNF-α) and interleukins (IL) IL-1β and IL-6 and increased IL-10. The gastroprotective activity of TA involved K  channels and the production of -SH, NO and PGE demonstrating multiple mechanisms of action. The results of the present study suggest that TA may be a gastroprotective agent counteracting oxidative and inflammatory stress.