Effect of polyunsaturated fatty acids on dexamethasone – induced gastric mucosal damage

• Published in: Prostaglandins, leukotrienes and essential fatty acids leukotrienes and essential fatty acids, 2000-02, Vol.62 (2), p.85-96
• Main Authors: Manjari, V., Das, U.N.
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Catalase - metabolism; Dexamethasone; Dietary Fats - administration & dosage; Dietary Fats - therapeutic use; Drug toxicity and drugs side effects treatment; Duodenum - metabolism; Fatty Acids - blood; Fatty Acids - metabolism; Fatty Acids, Unsaturated - administration & dosage; Fatty Acids, Unsaturated - therapeutic use; Fish Oils - administration & dosage; Fish Oils - therapeutic use; Gastric Mucosa - metabolism; Glucocorticoids; Glutathione Peroxidase - metabolism; Lipid Peroxides - blood; Lipid Peroxides - metabolism; Liver - metabolism; Male; Malondialdehyde - metabolism; Medical sciences; Nitric Oxide - blood; Nitric Oxide - metabolism; Pharmacology. Drug treatments; Phospholipids - blood; Phospholipids - metabolism; Rats; Rats, Wistar; Stomach Ulcer - chemically induced; Stomach Ulcer - prevention & control; Superoxide Dismutase - metabolism; Toxicity: digestive system
• ISSN: 0952-3278; 1532-2823
• DOI: 10.1054/plef.1999.0125

Background: Increased dietary intake of polyunsaturated fatty acids (PUFAs) is known to be associated with a decrease in the incidence of peptic ulcer disease possibly due to increase in the synthesis of prostaglandins. But, it is also likely that conversion of PUFAs to PGs may not always be required for gastric mucosal protection. Present study was designed to study the role of PUFAs in pathobiology of steroid induce gastric damage in rats. Methods: Wistar rats were treated with 5mg/kg bodyweight of dexamethasone to induce gastric mucosal ulcers. Effects of PUFAs was studied by supplementation of Fish oil (rich in n-3 EPA and DHA) and AA rich oil. Famotidine was used as a positive control. Generation of lipid peroxides, nitric oxide and the activity of anti-oxidant enzymes were also studied. Results: Dexamethasone induced ulceration was associated with changes in the phospholipid fatty acid profile, levels of lipid peroxidation products, nitric oxide and activity of anti-oxidant enzymes. The fatty acid profile showed an increase in LA and a decrease in other PUFAs like GLA, AA, EPA and DHA. When PUFAs were supplemented in the form of Fish oil and AA rich oil or when the animals were treated with H2-blocker, famotidine, there was a decrease in the incidence of ulceration in the animals associated with near normalization of changes in the phospholipid fatty acid profile. The levels of lipid peroxides, nitric oxide, and anti-oxidant activity also reverted to control values. Conclusions: Dexamethasone induced gastric ulceration was prevented by PUFAs. This is supported by the results of our earlier study where in it was noted that in patients with DU plasma lipid peroxides, nitric oxide and phospholipid fatty acid pattern and red cell antioxidant activity were altered similar to those seen in dexamethasone treated group of the present study. These abnormalities, similar to the PUFA treated groups of the present study, reverted to normalcy following treatment of the patients with lansoprazole, a proton pump inhibitor. Further, PUFAs are known to inhibit the growth of Helicobacter pylori in vitro. Hence, it is concluded that PUFAs, free radicals, nitric oxide and anti-oxidants play a significant role in the pathobiology of peptic ulcer.