Abstract
The effects of Vitamins C & E on Aspirin - induced gastric mucosal damage on gastric ulcer parameters and stomach oxidative stress markers were determined in acute and sub-acute studies in Wistar rats. Aspirin produced a significant (p<0.05) increase in gastric ulcer score in both studies. Vitamins C & E conferred protection in acute and sub-acute studies with preventive indices of 54 and 60% respectively. Histologically the gastric mucosa of animals in the sub-acute study showed a severe necrosis of the epithelial cells than observed in the acute study. Acute aspirin administration did not increase the stomach tissue Malondialdehyde (MDA) but sub-acute administration significantly (p<0.05) increased MDA, while vitamins C & E caused a significant (p<0.05) decrease below the level seen in normal controls. Aspirin in both studies significantly decreased Catalase activity. While acute aspirin exposure had no effect on Superoxide Dismutase (SOD) activity, sub-acute exposure raised it significantly (p<0.05). Administration of Vitamins C and E significantly increased SOD activity only in the acute study. Aspirin significantly decreased reduced Glutathione (GSH) in both studies and was reversed by Vitamin C and E. The level of GSH reductase (GSHRD) in the acute study was significantly decreased by aspirin but sub- acutely and prior treatment with vitamins C and E had no significant effect. Combine administration of vitamins C & E prior to intake of aspirin significantly prevented aspirin-induced gastric ulceration with decrease in some oxidative stress markers.
Highlights
Non-steroidal Anti-Inflammatory Drugs (NSAIDs) are the most commonly prescribed drugs because of their well-established efficacy in the treatment of pain, fever, inflammation and rheumatic disorders
Aspirin and other NSAIDs are associated with the occurrence of adverse Gastrointestinal (GI) side effects, ranging in severity from dyspeptic symptoms, gastrointestinal erosions and peptic ulcers to more serious complications such as bleeding or perforation (García and Barreales, 2007)
The established evidence that endogenous prostaglandins deficiency is associated with NSAIDsinduced gastroduodenal damage has provided important clues for the design of new anti-inflammatory drugs, which were expected to reduce toxicity
Summary
Non-steroidal Anti-Inflammatory Drugs (NSAIDs) are the most commonly prescribed drugs because of their well-established efficacy in the treatment of pain, fever, inflammation and rheumatic disorders. Their use has increased due to the use of aspirin in the prophylaxis of ischemic heart disease and thrombotic disorders (Dalen, 2006; Nema et al, 2009). The established evidence that endogenous prostaglandins deficiency is associated with NSAIDsinduced gastroduodenal damage has provided important clues for the design of new anti-inflammatory drugs, which were expected to reduce toxicity. Research for the possible additional factors that might be involved have reported the association of oxidative stress in NSAIDsinduced gastric damage but the mechanism involved is not clear
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