摘要
阿司匹林是最古老的非甾体抗炎药(非甾体抗炎药),和有时原因会被称为aspirin-exacerbated呼吸道疾病(AERD),它可以很严重。阿司匹林的副作用(阿斯匹林不耐受)也随着food-dependent运动性速发型过敏反应的患者中观察到,I型过敏疾病,aspirin-induced荨麻疹(AIU)。然而目标和阿斯匹林不耐受的机制仍然未知。没有AERD的动物或细胞模型,由于其病理生理机制仍然未知,但它认为抑制环氧酶的病原体导致增加免费花生四烯酸,这是代谢成半胱氨酰白三烯等(cysLTs)引起气道平滑肌收缩和哮喘症状。bed-tobench方法,确认临床讨论实验细胞模型,我们试图开发一个RBL-2H3 AERD使用激活细胞的细胞模型,大鼠肥大细胞细胞系。吲哚美辛(另一个非甾体抗炎药,也会引起AERD),提高体外cysLTs生产RBL-2H3细胞,虽然没有感应cysLTs生产没有炎症激活。因为这表明所有炎症细胞活化的前列腺素和cysLT新陈代谢应该应对非甾体抗炎药,然后我认为阿司匹林不应该分开随后的支气管收缩。证据的细胞机制非甾体抗炎药可以用于体外AERD的发展从bench-to-bed模型的方法。
关键词: 花生四烯酸代谢
Current Drug Targets
Title:Aspirin Intolerance: Experimental Models for Bed-to-Bench
Volume: 17 Issue: 16
Author(s): Masamichi Yamashita
Affiliation:
关键词: 花生四烯酸代谢
摘要: Aspirin is the oldest non-steroidal anti-inflammatory drug (NSAID), and it sometimes causes asthma-like symptoms known as aspirin-exacerbated respiratory disease (AERD), which can be serious. Unwanted effects of aspirin (aspirin intolerance) are also observed in patients with food-dependent exercise-induced anaphylaxis, a type I allergy disease, and aspirin-induced urticaria (AIU). However the target and the mechanism of the aspirin intolerance are still unknown. There is no animal or cellular model of AERD, because its pathophysiological mechanism is still unknown, but it is thought that inhibition of cyclooxygenase by causative agents leads to an increase of free arachidonic acid, which is metabolized into cysteinyl leukotrienes (cysLTs) that provoke airway smooth muscle constriction and asthma symptoms. As the bed-tobench approach, to confirm the clinical discussion in experimental cellular models, we have tried to develop a cellular model of AERD using activated RBL-2H3 cells, a rat mast cell like cell line. Indomethacin (another NSAID and also causes AERD), enhances in vitro cysLTs production by RBL-2H3 cells, while there is no induction of cysLTs production in the absence of inflammatory activation. Since this suggests that all inflammatory cells with activation of prostaglandin and cysLT metabolism should respond to NSAIDs, and then I have concluded that aspirin intolerance should be separated from subsequent bronchoconstriction. Evidence about the cellular mechanisms of NSAIDs may be employed for development of in vitro AERD models as the approach from bench-to-bed.
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Masamichi Yamashita , Aspirin Intolerance: Experimental Models for Bed-to-Bench, Current Drug Targets 2016; 17 (16) . https://dx.doi.org/10.2174/1389450117666161005152327
DOI https://dx.doi.org/10.2174/1389450117666161005152327 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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