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首页> 外文期刊>Clinical and experimental allergy : >Effects of celecoxib on major prostaglandins in asthma.
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Effects of celecoxib on major prostaglandins in asthma.

机译：塞来昔布对哮喘中主要前列腺素的影响。

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BACKGROUND: Prostaglandin (PG) D(2) is a pro-inflammatory and bronchoconstrictive mediator released from mast cells, and is currently evaluated as a new target for treatment of asthma and rhinitis. It is not known which cyclooxygenase (COX) isoenzyme catalyses its biosynthesis in subjects with asthma. OBJECTIVES: Primarily, to assess whether treatment with the COX-2 selective inhibitor celecoxib inhibited biosynthesis of PGD(2) , monitored as urinary excretion of its major tetranor metabolite (PGDM). Secondarily, to determine the effects of the treatment on biosynthesis of PGE(2) , thromboxane A(2) and PGI(2) , also measured as major urinary metabolites. METHODS: Eighteen subjects with asthma participated in a cross-over study where celecoxib 200mg or placebo were given b.i.d. on 3 consecutive days following 2 untreated baseline days. Six healthy controls received active treatment with the same protocol. Urinary excretion of the eicosanoid metabolites was determined by liquid chromatography/tandem mass spectrometry (LC/MS/MS). Lung function was followed as FEV(1) and airway inflammation as fraction of exhaled nitric oxide (F(E) NO). RESULTS: Celecoxib treatment inhibited urinary excretion of PGEM by 50% or more in subjects with asthma and healthy controls, whereas there was no significant change in the excretion of PGDM. In comparison with the healthy controls, the subjects with asthma had higher baseline levels of urinary PGDM but not of PGEM. The 3-day treatment did not cause significant changes in FEV(1) or F(E) NO. CONCLUSION AND CLINICAL RELEVANCE: Biosynthesis of PGD(2) was increased in subjects with asthma and its formation is catalysed predominantly by COX-1. By contrast, COX-2 contributes substantially to the biosynthesis of PGE(2) . The asymmetric impact of celecoxib on prostanoid formation raises the possibility of long-term adverse consequences of COX-2 inhibition on airway homeostasis by the decreased formation of bronchodilator PGs and maintained production of increased levels of bronchoconstrictor PGs in asthmatics.
机译：背景：前列腺素（PG）D（2）是从肥大细胞释放的促炎性支气管收缩介质，目前被评估为治疗哮喘和鼻炎的新靶标。尚不清楚在哮喘患者中哪种环氧合酶（COX）同工酶能催化其生物合成。目的：首先，评估COX-2选择性抑制剂塞来昔布治疗是否抑制了PGD（2）的生物合成，监测其主要四氟甲酸酯代谢物（PGDM）的尿排泄。其次，要确定治疗对PGE（2），血栓烷A（2）和PGI（2）的生物合成的影响，血栓素A（2）和PGI（2）也是主要的尿代谢产物。方法：18名哮喘患者参加了一项交叉研究，在该研究中b.i.d.给予200mg塞来昔布或安慰剂。在2个未处理的基准日之后连续3天。六个健康对照组接受了相同方案的积极治疗。通过液相色谱/串联质谱法（LC / MS / MS）测定类花生酸代谢产物的尿排泄。肺功能为FEV（1），气道炎症为呼出的一氧化氮（F（E）NO）。结果：塞来昔布治疗在患有哮喘和健康对照的受试者中将PGEM的尿排泄抑制了50％或更多，而PGDM的排泄没有明显变化。与健康对照相比，患有哮喘的受试者的尿中PGDM基线水平较高，但PGEM没有。为期3天的治疗并未引起FEV（1）或F（E）NO的显着变化。结论和临床意义：哮喘患者中PGD（2）的生物合成增加，其形成主要由COX-1催化。相比之下，COX-2实质上有助于PGE（2）的生物合成。塞来昔布对前列腺素形成的不对称影响通过减少支气管扩张剂PG的形成并维持哮喘患者支气管收缩剂PG的水平升高而增加了COX-2抑制气道稳态的长期不良后果的可能性。

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