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糖皮质激素在 NSAID 诱导的胃病中的胃保护作用。

Gastroprotective role of glucocorticoids during NSAID-induced gastropathy.

机构信息

Laboratory of Experimental Endocrinology, Pavlov Institute of Physiology, Russian Academy of Sciences, nab. Makarova 6, St. Petersburg 199034, Russia.

出版信息

Curr Pharm Des. 2013;19(1):29-33. doi: 10.2174/13816128130106.

Abstract

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.

摘要

非甾体抗炎药(NSAIDs)对广泛存在的胃溃疡疾病有重要贡献。虽然已经提出了几种因素作为 NSAIDs 诱导的胃损伤的发病机制,但据信前列腺素缺乏在这种损伤的发病机制中起着关键作用。在前列腺素缺乏期间,其他防御机制可能会发挥作用以减轻 NSAID 诱导的胃病。根据我们的结果,NSAIDs 与应激相似,会诱导糖皮质激素产生增加,这反过来有助于胃黏膜抵抗这些药物的有害作用。在本文中,我们回顾了我们的实验数据,表明糖皮质激素可能作为天然防御因素在 NSAID 治疗期间发挥作用,以维持胃黏膜的完整性,并可能减轻 NSAID 诱导的胃病。

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