Volume 22, Issue 1 (Winter 2018)                   Physiol Pharmacol 2018, 22(1): 48-53 | Back to browse issues page

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Nazariani N, Mard S A, Nasri S, Veisi A. Gastroprotective effect of sodium hydrosulfide against indomethacin-induced gastric ulcer in diabetic rats. Physiol Pharmacol 2018; 22 (1) :48-53
URL: http://ppj.phypha.ir/article-1-1322-en.html
Abstract:   (3077 Views)

Introduction: The incidence rate of gastric erosions and ulcers in diabetic patients are higher due to failure of mucosal antioxidant defense and maintain enough blood flow. The present study evaluated the gastro-protective effect of sodium hydrosulfide (NaHS) against indomethacin-induced gastric lesions in diabetic rats. Methods: In order to test anti-ulcer activity of NaHS against indomethacin, four diabetic groups of rats including diabetic control and 3 NaHS-treated groups received a single dose of physiologic saline or NaHS at 320, 640 and 1280 μg/kg respectively, 30 min before ulcer induction by indomethacin. Five hours later, the animals were killed and their stomachs were removed for macroscopically and microscopically evaluations. In order to evaluate the antacid effect of NaHS, 4 groups of diabetic rats received physiologic saline or NaHS at 320, 640 and 1280 μg/kg and 30 min later anesthetized, underwent a midline laparotomy and then their pylorus ligated. Five hours later, the animals were killed, their stomachs were removed and pH of gastric effluents were measured. Results: Indomethacin induced gastric lesions in glandular part of the stomach. NaHS at 640 and 1280 μg/kg significantly decreased the indomethacin-induced gastric lesions in diabetic rats. The pH of gastric effluents and mucus content increased by NaHS at doses of 640 and 1280 μg/kg. Macroscopic and microscopic observations showed that mucosal erosions induced by indomethacin were significantly inhibited by NaHS. Conclusion: results suggest NaHS through decreasing the rate of gastric acid output and increasing the mucus production, protected the gastric mucosa against indomethacin-induced gastric lesions in diabetic rats.

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