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儿童氧化应激与支气管哮喘——原因还是后果?

Oxidative Stress and Bronchial Asthma in Children-Causes or Consequences?

作者信息

Jesenak Milos, Zelieskova Maria, Babusikova Eva

机构信息

Jessenius Faculty of Medicine, Department of Pediatrics, Comenius University in Bratislava, University Hospital, Martin, Slovakia.

Jessenius Faculty of Medicine, Department of Medical Biochemistry, Comenius University in Bratislava, Martin, Slovakia.

出版信息

Front Pediatr. 2017 Jul 24;5:162. doi: 10.3389/fped.2017.00162. eCollection 2017.

Abstract

Bronchial asthma is one of the most common chronic inflammatory diseases of the airways. In the pathogenesis of this disease, the interplay among the genes, intrinsic, and extrinsic factors are crucial. Various combinations of the involved factors determine and modify the final clinical phenotype/endotype of asthma. Oxidative stress results from an imbalance between the production of reactive oxygen species and reactive nitrogen species and the capacity of antioxidant defense mechanisms. It was shown that oxidative damage of biomolecules is strongly involved in the asthmatic inflammation. It is evident that asthma is accompanied by oxidative stress in the airways and in the systemic circulation. The oxidative stress is more pronounced during the acute exacerbation or allergen challenge. On the other hand, the genetic variations in the genes for anti-oxidative and pro-oxidative enzymes are variably associated with various asthmatic subtypes. Whether oxidative stress is the consequence of, or the cause for, chronic changes in asthmatic airways is still being discussed. Contribution of oxidative stress to asthma pathology remains at least partially controversial, since antioxidant interventions have proven rather unsuccessful. According to current knowledge, the relationship between oxidative stress and asthmatic inflammation is bidirectional, and genetic predisposition could modify the balance between these two positions-oxidative stress as a cause for or consequence of asthmatic inflammation.

摘要

支气管哮喘是最常见的气道慢性炎症性疾病之一。在该疾病的发病机制中,基因、内在因素和外在因素之间的相互作用至关重要。相关因素的各种组合决定并改变哮喘的最终临床表型/内型。氧化应激源于活性氧和活性氮的产生与抗氧化防御机制能力之间的失衡。研究表明,生物分子的氧化损伤与哮喘炎症密切相关。显然,哮喘在气道和体循环中均伴有氧化应激。在急性加重期或过敏原激发期间,氧化应激更为明显。另一方面,抗氧化和促氧化酶基因的遗传变异与各种哮喘亚型存在不同程度的关联。氧化应激是哮喘气道慢性变化的结果还是原因仍在讨论中。氧化应激对哮喘病理的作用至少部分存在争议,因为抗氧化干预已被证明效果不佳。根据目前的知识,氧化应激与哮喘炎症之间的关系是双向的,遗传易感性可能会改变这两个方面之间的平衡——氧化应激是哮喘炎症的原因还是结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4271/5523023/b2838784bf71/fped-05-00162-g001.jpg

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