Gastroprotective Effects of Nigella sativa (Black Seed) Oil on Serum Biochemical Markers and Gastric Histoarchitecture in Ethanol-Induced Gastric Ulceration in Wistar Rats
Aniah Julius Akomaye, Mohammed Ahmed Mirwa, James Rimamtsab, Inyang Bassey Atte
Asian Journal of Research and Reports in Gastroenterology · pp. 234–252 · Published 6 Aug 2026
10.9734/ajrrga/2026/v9i1224Abstract
Background: Peptic ulcer disease remains a major global gastrointestinal disorder, and ethanol-induced gastric ulceration in rodents is a well-validated model for studying mucosal injury driven by oxidative stress, inflammation, and disruption of gastric mucosal defences. Conventional therapies such as proton pump inhibitors are effective but are increasingly associated with long-term adverse effects, prompting interest in natural gastroprotective agents such as black seed (Nigella sativa) oil, whose principal constituent, thymoquinone, possesses antioxidant and anti-inflammatory properties. Objective: This study investigated the gastroprotective effects of black seed oil on serum biochemical markers (total protein, albumin, globulin, and pepsinogen) and gastric histological architecture in ethanol-induced gastric ulceration in Wistar rats compared with the standard anti-ulcer drug omeprazole. Methods: Gastric ulceration was induced in Wistar rats by oral administration of absolute ethanol. Animals were pretreated with black seed oil at doses of 1 mL/kg body weight (BW) and 2 mL/kg BW, or with omeprazole (30 mg/kg BW) before ulcer induction; untreated ulcer and normal control groups were also included. Serum concentrations of total protein, albumin, globulin, and pepsinogen were determined, and gastric tissues were examined histologically for mucosal architecture and integrity. Results: Untreated ulcerated rats showed significantly elevated serum total protein, globulin, and pepsinogen concentrations and a significantly reduced albumin concentration relative to normal controls, together with severe histological mucosal erosion, gastric pit enlargement, and disruption of normal gastric architecture. Pretreatment with black seed oil at both doses significantly reduced total protein, globulin, and pepsinogen concentrations towards normal values and markedly improved gastric histological architecture, with the 1 mL/kg BW dose producing the most consistent biochemical and histological restoration, including a significant increase in serum albumin. The 2 mL/kg BW dose showed comparatively less improvement in albumin concentration and mild residual histological changes, suggesting a non-linear dose-dependent response. Conclusion: Black seed oil, particularly at 1 mL/kg BW, conferred significant biochemical and histological protection against ethanol-induced gastric ulceration and was comparable in several respects to omeprazole. These findings support the potential of black seed oil as a natural, effective adjunct or alternative to conventional pharmacological agents in the prevention and management of gastric ulcer disease, while highlighting the need for further dose-optimisation studies.
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