Besides the preventive effect of aspirin on cerebrocardiovascular diseases, aspirin has adverse effects, especially on the gastrointestinal system and kidneys. Especially, a recent advancement in endoscopy revealed that aspirin-induced small intestinal mucosal injury is considerably higher than previously believed. However, the mechanism of this phenomenon is not clear yet. Moreover, effective prophylaxis does not exist. First, we investigated the cytotoxic effect of aspirin on the intestinal epithelial cell line in rats at a high concentration, and found that aspirin significantly decreased heat shock protein 70 expression, increased reactive oxygen species production, and increased epithelial cell apoptosis. These phenomena were prevented by the increment of heat shock protein 70 expression. Next, we investigated the effect of a lower concentration of aspirin on epithelial cell permeability, and found that aspirin significantly increased reactive oxygen species production, decreased tight junction protein expression, and increased epithelial permeability. These phenomena were suppressed by an antioxidant. Finally, we investigated the role of intestinal mucus on aspirin-induced mucosal damage using an in vivo model, and found that mucus prevented a high concentration of aspirin-induced mucosal damage. The investigation of chronic users of aspirin revealed that mucus-increasing therapy might be useful for preventing aspirin-induced small intestinal mucosal injury.
Keywords: Acetyl salycilic acid; apoptosis; mucusIntroduction; permeability; small intestine.