Thymoquinone and caffeic acid phenethyl ester mitigate experimental ulcerative colitis: a biochemical and...

To establish an acetic acid-induced acute ulcerative colitis model in rats and to evaluate the clinical, biochemical, and histopathological effects of thymoquinone (TQ) and caffeic acid phenethyl ester (CAPE) in this model.

Forty male Wistar albino rats (190-303 g) were randomly assigned to five groups (n = 8). All groups except the control received rectal acetic acid (4%) to induce colitis. Group 1 (control) received intraperitoneally (IP) 0.9% saline for five days. Group 2 (colitis) received IP 10% ethanol (vehicle for CAPE). Group 3 (TQ) received IP thymoquinone (10 mg/kg/day). Group 4 (CAPE) received IP caffeic acid phenethyl ester (10 µmol/kg/day). Group 5 (TQ+CAPE) received both agents at the same doses. On day 5, animals were euthanized, and colon and serum samples were collected for biochemical and histopathological analysis.

Significant differences were observed in the disease activity index, tumor necrosis factor-α, catalase, glutathione peroxidase, interleukin-10, and malondialdehyte indicating a balance between oxidant and antioxidant parameters. CAPE was found to have a greater anti-inflammatory effect than TQ histopathologically. The combined administration of CAPE and TQ mitigated oxidative stress as demonstrated by decreased oxidative stress biomarkers and improved antioxidant protection.

Both CAPE and TQ demonstrated anti-inflammatory and antioxidant effects in an acetic acid-induced colitis model, with CAPE showing greater histological improvement. Their combined administration yielded additional benefits in oxidative stress reduction. These findings suggest that CAPE and TQ, particularly in combination, may hold promise as adjunctive agents in colitis management and warrant further investigation.