首页> 美国卫生研究院文献>Clinical and Developmental Immunology >Suppression of Leukotriene B4 Generation by Ex-vivo Neutrophils Isolated from Asthma Patients on Dietary Supplementation with Gammalinolenic Acid-containing Borage Oil: Possible Implication in Asthma
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Suppression of Leukotriene B4 Generation by Ex-vivo Neutrophils Isolated from Asthma Patients on Dietary Supplementation with Gammalinolenic Acid-containing Borage Oil: Possible Implication in Asthma

机译:饮食中补充含γ亚麻酸的琉璃苣油对哮喘患者的离体中性粒细胞产生白三烯B4的抑制作用:对哮喘的可能影响

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摘要

Dietary gammalinolenic acid (GLA), a potent inhibitor of 5-lipoxygenase (5-LOX) and suppressor of leukotriene B4 (LTB4), can attenuate the clinical course of rheumatoid arthritics, with negligible side effects. Since Zileuton, also an inhibitor of 5-LOX, attenuates asthma but with an undesirable side effect, we investigated whether dietary GLA would suppress biosynthesis of PMN-LTB4 isolated from asthma patients and attenuate asthma. Twenty-four mild-moderate asthma patients (16–75 years) were randomized to receive either 2.0 g daily GLA (borage oil) or corn oil (placebo) for 12 months. Blood drawn at 3 months intervals was used to prepare sera for fatty acid analysis, PMNs for determining phospholipid fatty acids and for LTB4 generation. Patients were monitored by daily asthma scores, pulmonary function, and exhaled NO. Ingestion of daily GLA (i) increased DGLA (GLA metabolite) in PMN-phospholipids; (ii) increased generation of PMN-15-HETrE (5-LOX metabolite of DGLA). Increased PMN-DGLA/15-HETrE paralleled the decreased PMN generation of proinflammatory LTB4. However, the suppression of PMN-LTB4 did not reveal statistically significant suppression of the asthma scores evaluated. Nonetheless, the study demonstrated dietary fatty acid modulation of endogenous inflammatory mediators without side effects and thus warrant further explorations into the roles of GLA at higher doses, leukotrienes and asthma.
机译:饮食中的亚麻酸(GLA)是有效的5-脂氧合酶(5-LOX)抑制剂和白三烯B4(LTB4)抑制剂,可减轻类风湿关节炎的临床病程,且副作用可忽略不计。由于Zileuton(也是5-LOX的抑制剂)可减轻哮喘,但具有不良副作用,因此我们研究了饮食GLA是否会抑制从哮喘患者中分离出的PMN-LTB4的生物合成并减轻哮喘。 24名轻度-中度哮喘患者(16-75岁)被随机分配接受每日2.0 g GLA(琉璃苣油)或玉米油(安慰剂)治疗12个月。每隔三个月抽取一次血液,用于制备血清以进行脂肪酸分析,使用PMN来测定磷脂脂肪酸和生成LTB4。通过每日哮喘评分,肺功能和呼出气NO监测患者。每天摄入GLA(i)PMN磷脂中的DGLA(GLA代谢产物)增加; (ii)增加PMN-15-HETrE(DGLA的5-LOX代谢产物)的产生。 PMN-DGLA / 15-HETrE的增加与促炎性LTB4的PMN产生的减少平行。但是,对PMN-LTB4的抑制并未显示出对所评估的哮喘评分的统计学显着抑制。尽管如此,该研究表明膳食脂肪酸调节内源性炎症介质没有副作用,因此有必要进一步研究高剂量GLA,白三烯和哮喘的作用。

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