Gastro-protective Effect of Corn Diet against Indomethacin Induced Ulceration in Experimental Rats

Introduction: One of the most prevalent gastrointestinal ailments is gastric ulcer, which is caused by an imbalance between protective and aggressive factors. Zea mays Corn is a significant cereal crop containing natural phytochemical substances that are sources of nourishment. The methanolic extract of Corn, according to a previous study, lowers stomach acidity and inhibits the percentage of gastric ulceration with no knowledge on the mechanisms involved.

Aim: This study investigated the underlying gastroprotective mechanisms of the Corn diet (ZD).

Materials and Methods: Sixty male Wistar rats were used, randomly grouped into 6; 1(Normal control), 2(Ulcerated control), 3, 4, 5 (prefed with ZD -55%, 65%, 75%) and 6 (cimetidine- 25mg/kg) for 28 days. Gastric ulcer was induced by oral administration of indomethacin (40mg/kg) and animals were sacrificed after 4 hours. The stomach was excised and cleaned, it was then homogenized and centrifuged for biochemical assays.

Results: There is a significant reduction in gastric ulcer area in all treated groups. Significant increase in gastric tissue mucin content and gastric mucosal SOD, NO and PGE2 levels and significant reduction in the MDA was observed in the ZD and cimetidine group. Histological evaluation showed tubular glands closely packed and separated from each other by laminar propia, however there is mild presence of inflammatory cells within the laminar propia in the ZD groups compared to ulcerated control group that showed moderate oedema with infiltration of inflammatory cells with mild vascular congestion in the mucosa. There is significant reduction in the macroscopic gastric mucosal lesions with percentage inhibition of 90%, 92%, 90% and 92% in the ZD (55%, 65% and 75%) and cimetidine group respectively.

Conclusion: Results obtained from this study suggests that Zm diet may have anti-ulcerogenic properties by enhancing antioxidant enzymes as well as, nitric oxide and prostaglandin E2 mechanisms.