BACKGROUND: Numerous studies have shown that use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with various gastric mucosal lesions, collectively referred to as NSAID gastropathy, but the detailed mechanism is still not properly understood. L-carnitine, a vitamin-like substance, is a naturally occurring enzymatic antioxidant with a potent free oxygen radical quencher and scavenger capacity; it protects the biological membranes against lipid peroxidation. It has recently been shown that L-carnitine has a gastroprotective effect on gastric mucosa. To our knowledge, the role of L-carnitine on NSAIDs-induced gastric mucosal injury is undefined. AIM: The aim of the present study was to determine the gastroprotective effect of L-carnitine on indomethacin-induced gastric mucosal lesions in the rat stomachs. MATERIAL AND METHODS: In our study, gastric mucosal injury was induced by the intragastric administration of indomethacin (30 mg/kg). L-carnitine (10, 50, 100 mg/kg) was given to rats by gavage 30 min before the indomethacin administration. The animals were killed 3 h after administration of indomethacin. The stomach of each animal was removed. Mucosal damage was evaluated with macroscopic study and histopathologically. RESULTS: The intragastric administration of indomethacin induced hyperemia and hemorrhagic erosions in the rat stomachs. L-carnitine significantly prevented gastric ulcerogenesis induced by indomethacin and decreased the ulcer index macroscopically and histopathologically. CONCLUSION: L-carnitine decreases indomethacin-induced gastric mucosal injury and this gastroprotective effect may be attributed to its well-known antioxidant effect.
BACKGROUND: Numerous studies have shown that use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with various gastric mucosal lesions, collectively referred to as NSAID gastropathy, but the detailed mechanism is still not properly understood. L-carnitine, a vitamin-like substance, is a naturally occurring enzymatic antioxidant with a potent freeoxygen radical quencher and scavenger capacity; it protects the biological membranes against lipid peroxidation. It has recently been shown that L-carnitine has a gastroprotective effect on gastric mucosa. To our knowledge, the role of L-carnitine on NSAIDs-induced gastric mucosal injury is undefined. AIM: The aim of the present study was to determine the gastroprotective effect of L-carnitine on indomethacin-induced gastric mucosal lesions in the rat stomachs. MATERIAL AND METHODS: In our study, gastric mucosal injury was induced by the intragastric administration of indomethacin (30 mg/kg). L-carnitine (10, 50, 100 mg/kg) was given to rats by gavage 30 min before the indomethacin administration. The animals were killed 3 h after administration of indomethacin. The stomach of each animal was removed. Mucosal damage was evaluated with macroscopic study and histopathologically. RESULTS: The intragastric administration of indomethacin induced hyperemia and hemorrhagic erosions in the rat stomachs. L-carnitine significantly prevented gastric ulcerogenesis induced by indomethacin and decreased the ulcer index macroscopically and histopathologically. CONCLUSION:L-carnitine decreases indomethacin-induced gastric mucosal injury and this gastroprotective effect may be attributed to its well-known antioxidant effect.