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哮喘患者内皮型一氧化氮合酶和血管紧张素转换酶的基因多态性

Gene polymorphisms of endothelial nitric oxide synthase and angiotensin-converting enzyme in patients with asthma.

作者信息

Lee Y C, Cheon K T, Lee H B, Kim W, Rhee Y K, Kim D S

机构信息

Department of Internal Medicine, Research Institute of Clinical Medicine, Chonbuk National University Medical School, Chonju, South Korea.

出版信息

Allergy. 2000 Oct;55(10):959-63. doi: 10.1034/j.1398-9995.2000.00724.x.

Abstract

BACKGROUND

Nitric oxide, including that produced by endothelial constitutive nitric oxide synthase (ecNOS), may regulate vascular and airway tone in the lungs and may influence various aspects of airway homeostasis. Angiotensin-converting enzyme (ACE) is expressed at high levels in the lungs and plays a role in the metabolism of angiotensin II, bradykinin, and substance P, all of which are potentially involved in the pathogenesis of asthma. An insertion-deletion polymorphism of the ACE gene has been shown to be associated with enzyme activity levels of ACE. To examine the possible involvement of the ecNOS and/or ACE genes as the genetic basis of bronchial asthma, we investigated whether there was any association between bronchial asthma and polymorphisms of the ecNOS and/or ACE genes.

METHODS

A total of 310 patients with bronchial asthma and 121 healthy subjects took part in this study. The ecNOS and ACE genotypes were determined in all subjects by polymerase chain reaction.

RESULTS

  1. The distribution of one genotype (bb) of ecNOS was significantly higher in the asthma group than in the control population. 2) The ACE genotype distribution was not significantly different between the control and the asthma groups. 3) In asthmatic patients, the ACE and ecNOS genotype distribution did not differ significantly among groups of patients with different severities of asthma.

CONCLUSIONS

These results suggest that polymorphisms of the ecNOS gene, but not the ACE gene, may be associated with the development of asthma. However, the severity of asthma may not be influenced by polymorphisms of the ecNOS and ACE genes.

摘要

背景

一氧化氮,包括由内皮型一氧化氮合酶(ecNOS)产生的一氧化氮,可能调节肺部血管和气道张力,并可能影响气道稳态的各个方面。血管紧张素转换酶(ACE)在肺部高水平表达,在血管紧张素II、缓激肽和P物质的代谢中起作用,所有这些都可能参与哮喘的发病机制。ACE基因的插入-缺失多态性已被证明与ACE的酶活性水平相关。为了研究ecNOS和/或ACE基因作为支气管哮喘遗传基础的可能参与情况,我们调查了支气管哮喘与ecNOS和/或ACE基因多态性之间是否存在关联。

方法

共有310例支气管哮喘患者和121名健康受试者参与了本研究。通过聚合酶链反应测定所有受试者的ecNOS和ACE基因型。

结果

1)哮喘组中ecNOS的一种基因型(bb)的分布显著高于对照组。2)对照组和哮喘组之间的ACE基因型分布没有显著差异。3)在哮喘患者中,不同哮喘严重程度组之间的ACE和ecNOS基因型分布没有显著差异。

结论

这些结果表明,ecNOS基因的多态性而非ACE基因的多态性可能与哮喘的发生有关。然而,哮喘的严重程度可能不受ecNOS和ACE基因多态性的影响。

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