Gastroprotective effects of hydrogen sulfide, carbon monoxide and nitric oxide on an experimental ulcer model in rats

Abstract

Background/Aim: Gastric mucosal injury induced by several agents such as ethanol, stress or nonsteroidal anti-inflammatory drugs (NSAIDs) is a common severe disorder. Hydrogen sulfide (H2S), carbon monoxide (CO) and nitric oxide (NO) are gaseous autacoids that are endogenously produced in mammalian tissues. Recently, several studies confirmed that H2S, CO and NO play a role in gastroprotection. Our work aimed to evaluate and compared the gastroprotective effects of H2S, CO and NO on ethanol-, indomethacin- and stress-induced rat ulcer models. Methods: The effects of NaHS (5 mg/kg), CORM-2 (5 mg/kg) and L-arginine (100 mg/kg) were investigated on gastric ulcer models induced by ethanol (1 ml 96% i.g.), stress (cold+immobility) and indomethacin (40 mg/kg i.g.). The ulcer index, gastric mucus secretion, free and total acidity, and levels of TNF-α, PGE2, MDA GSH, COX-1, COX-2 were measured. Results: NaHS and CORM-2 decreased the increased TNF-α and MDA levels in ethanol-induced ulcer. L-arginine reduced mucin secretion, TNF-α and GSH levels in stress-induced gastric ulcer. Conclusion: The present study showed that H2S and CO may have gastroprotective activity against ethanol-induced ulcers and NO may be gastroprotective against stress-induced ulcers.