| [ Summary ] |
The investigation of gastric mucosal inflammation, known as gastritis, has been focused on the initial pathogenesis leading to mucosal damage caused by non-steroidal anti-inflammatory drugs (NSAIDs), even though they have a potent anti-inflammatory effect on other inflammatory locations. Therefore, it is important to elucidate the mechanisms of gastric mucosal inflammation induced by NSAIDs. Prostaglandin (PG) E2 and I2, and leukotriene (LT) C4 and B4, metabolites of arachidonic acid, are involved in the homeostasis of gastric tissues such as the mucosal defence system which reacts against some topical irritants and the maintenance of gastric mucosal blood flow in stressed conditions. Recently, an imbalance in PG/LT synthesis via NSAIDs, the most potent inhibitors of PG synthetase, has been reported to be associated with gastric inflammation.In this chapter, we will discuss in the metabolism of arachidonic acid, in particular we will review the current knowledge available about the involvement of microcirculation of the gastric mucosa, inflammatory cytokines, adhesion molecules, and polymorphonuclear cells in the pathophysiological and molecular biological mechanisms affecting gastric mucosal inflammation, caused by NSAIDs. |