Some Biochemical Changes Followed Experimental Gastric Ulceration

Gastric ulceration is a discontinuity in gastric mucosa, usually occurs due to imbalance between the gastric mucosal protective factors, that is called gastric mucosal barrier, and the aggressive factors, to which the mucosa is exposed. This study was carried out on sixty male Sprague-Dowely rats (12- 16 weeks old) allocated into two groups. The first control group and the second Gastric lesion group which induced by oral administration of a single daily dose of aspirin at a dose of 300 mg/kg body weight for 7 consecutive-days (6% aspirin solution will be prepared and each rat will be given 5 ml of that solution/kg body weight). Blood is collected 1, 2 and 3 weeks after induction of gastric ulceration. Significant increase in serum copper, nitric oxide, and prostaglandin E2 all over the period of experiment. Significant decrease in erythrocyte superoxide dismutase (t-SOD) activities, serum (calcium, phosphorus, glucose and insulin) levels. Non-significant changes in serum sodium and potassium levels are obtained.





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