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The healing activities of black tea (BT) and the theaflavins (TF) against the indomethacin-induced stomach ulceration were studied in a mouse model. Indomethacin (18 mg/kg, p.o.) administration induced maximum ulceration in the glandular portion of the gastric mucosa on the 3rd day, accompanied by increased lipid peroxidation and protein oxidation, depletion of thiol-defense and mucin, as well as reduced expressions of cyclooxygenases (COX) and prostaglandin (PG) E synthesis in the gastric tissues, and plasma total antioxidant status of mice. Treatment with BT (40 mg/kg), TF (1 mg/kg), and omeprazole (3 mg/kg) produced similar (74%–76%) ulcer healing, as revealed from the histopathological studies. Treatment with all the above samples reversed the adverse oxidative effects of indomethacin significantly. BT and TF also enhanced the PGE synthesis by augmenting the expressions of COX 1 and 2, but did not modulate acid secretion.

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Management of the gastric toxicity of non-steroidal anti-inflammatory drugs (NSAIDs) remains a crucial problem because the commercially available drugs have side effects and are often expensive. Therefore, we examined the potential of the green tea-derived polyphenol epigallocatechin gallate (EGCG) to treat indomethacin-induced stomach ulcers in mice. Administration of indomethacin (18 mg/kg, po) to mice induced ulceration in the glandular portion of the gastric mucosa, accompanied by increased lipid peroxidation (LPO) and protein oxidation and reductions in thiol defense, mucin, cyclooxygenase (COX) expression and prostaglandin (PG) synthesis in the gastric tissues. Daily oral administration of EGCG (2 mg/kg) or omeprazole (3 mg/kg) for 3 days produced similar (≈ 72-75%, p < 0.001) beneficial effects on the acute gastric ulceration. Treatment with the test samples partially reversed all the adverse oxidative effects of indomethacin. In addition, EGCG, but not omeprazole, enhanced expression of the COX isoforms and PG synthesis. The results suggest that the non-toxic and inexpensive tea polyphenol EGCG may be an excellent candidate for further evaluation as a potent anti-ulcer drug.

The modulation of the cyclooxygenase-independent pathway by black tea (BT) and its constituent theaflavins (TFs) during their healing action against indomethacin-induced stomach ulceration in mice was investigated. On the 3(rd) day of its administration, indomethacin (18 mg/kg) induced maximum stomach ulceration, which was associated with increased myeloperoxidase (MPO) activity (93.3%, p<0.001), and inducible nitric oxide synthase (iNOS) expression (1.6-fold, p<0.001), along with augmented levels of serum nitrite (1.5-fold, p<0.001), selectins and cell adhesion molecules (CAMs), as well as reduced endothelial nitric oxide synthase (eNOS) expression (60%, p<0.001). Treatment with BT (40 mg/kg) and TF (1 mg/kg) for 3 days reversed these parameters and provided excellent (78-81%) ulcer healing. However, alterations of NOS expressions and levels of selectins and CAMs were only partially responsible for the excellent healing capacity (∼80%) of omeprazole (3 mg/kg × 3 days).

The modulation of the cyclooxygenase-independent pathway by the green tea-derived polyphenol, epigallocatechin gallate (EGCG) during its healing action against indomethacin (IND)-induced stomach ulceration in mice was investigated. On the 3rd day of its administration, IND (18 mg kg(-1)) induced maximum stomach ulceration which was associated with increased myeloperoxidase (MPO) activity (2.1-fold, p < 0.001), and inducible nitric oxide synthase (iNOS) expression (2.5-fold, p < 0.001), along with augmented levels of serum nitrite (1.3-fold, p < 0.001), selectins and cell adhesion molecules (CAMs), as well as reduced endothelial nitric oxide synthase (eNOS) expression (53%, p < 0.001). Treatment with EGCG (2 mg kg(-1)) and omeprazole (3 mg kg(-1)) for 3 days reversed these parameters, and provided excellent (76-77%) ulcer healing.

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