Protective effect of okra seed oil on acute gastric ulcer in mice

To investigate the protective effect of the seed oil of Abelmoschus esculentus on gastric ulcer, two acute gastric ulcer mice models were established by intragastric administration of aspirin or absolute ethanol, respectively. Clinical index of ulcer area, ulcer index, gastric volume, gastric pH value, free acidity, total acidity, and histopathological assessment were measured to evaluate the injuries of gastric ulcer and the protective effect of okra seed oil. In order to comprehensively uncover the possible underlying mechanism, a series of biochemical assays were also performed, including serum TNF-α, IL-6, IL-10 and Tbil, NO, MPO and SOD in the stomach included. Moreover, the ALT, AST and ALP in the liver of mice were also tested to evaluate the possible hepatic toxicity of the seed oil. The results indicated that the seed oil of A. esculentus exerted protective effect in ethanol-induced gastric ulcer mice by reducing the ulcer area and ulcer index, declining the free and total acidity, and increasing the pH value of gastric content. Histopathological observation showed the gastric mucosa of the acute gastric ulcer mice induced by alcohol was incomplete and severely damaged, with submucosal edema and nuclear pyknosis, as well as glandular structure disappearing, compared with that of normal mice. What′s more, a number of inflammatory cell infiltration occured in the gastric mucosa of alcohol-model mice, with messes of neutrophils, lymphocytes, eosinophils and plasma cells. Okra seed oil could improve the damaged structure of the gastric mucosa and gland caused by ethanol, but could not ameliorate the condensation of nucleus and infiltration of inflammatory cells. Biochemical analysis revealed that the seed oil of A. esculentus could counteract the damage induced by ethanol via decreasing Tbil and TNF-α in serum, decreasing NO and myeloperoxidase, and increasing SOD in stomach. Meanwhile, okra seed oil exhibited protective effect in aspirin-induced gastric ulcer mice by increasing the gastric content pH, and reducing free and total acidity. Compared with the control group, the gastric mucosa of aspirin-model group showed multifocal coagulation necrosis, sheet edema and infiltration of inflammatory cells by histopathological assessment. Compared with the aspirin-model group, the soybean oil group and okra seed oil group could ameliorate the inflammatory cell infiltration. Biochemical analysis revealed that okra seed oil could counteract the injury induced by aspirin via decreasing TNF-α and IL-6, and increasing IL-10 in serum, decreasing NO and MPO and increasing SOD in stomach. In a word, the okra seed oil exerted protective effect on acute gastric ulcer by anti-inflammation, anti-oxidation and hepatocyte protection. The okra seed oil deserves further development and utilization.