Nonsteroidal anti-inflammatory drugs (NSAIDs) make significant contributions to gastric ulcer disease which remains widespread.
Although several factors have been postulated as pathogenic elements of the gastric injury induced by NSAIDs, it is, however
believed that prostaglandin deficiency plays a critical role in the pathogenesis of this injury. During prostaglandin deficiency, other
defensive mechanisms might operate to attenuate NSAID-induced gastropathy. According to our results, NSAIDs, similar to stress, induce
an increase in glucocorticoid production that in turn helps the gastric mucosa to resist the harmful actions of these drugs. In this article,
we review our experimental data suggesting that glucocorticoids may play a role as natural defensive factors in maintaining the
integrity of the gastric mucosa during NSAID therapy and might operate to attenuate NSAID-induced gastropathy.
Keywords: Nonsteroidal anti-inflammatory drugs, indomethacin, aspirin, gastric erosion, the hypothalamic-pituitary-adrenocortical axis, glucocorticoids, gastroprotection, ulcer, injury, gastric mucosa
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