Laboratório de Farmacologia Funcional Prof. George Thomas, Instituto de Pesquisa em Fármacos e Medicamentos, Universidade Federal da Paraíba, João Pessoa, PB 58.051-900, Brazil.
Departamento de Fisiologia e Patologia, Centro de Ciências da Saúde, Universidade Federal da Paraíba, João Pessoa, PB 58.051-900, Brazil.
Oxid Med Cell Longev. 2021 Mar 3;2021:6692110. doi: 10.1155/2021/6692110. eCollection 2021.
Asthma is a chronic inflammatory disease of the airways related to epithelial damage, bronchial hyperresponsiveness to contractile agents, tissue remodeling, and luminal narrowing. Currently, there are many data about the pathophysiology of asthma; however, a new aspect has emerged related to the influence of reactive oxygen and nitrogen species (ROS and RNS) on the origin of this disease. Several studies have shown that an imbalance between the production of ROS and RNS and the antioxidant enzymatic and nonenzymatic systems plays an important role in the pathogenesis of this disease. Considering this aspect, this study is aimed at gathering data from the scientific literature on the role of oxidative distress in the development of inflammatory airway and lung diseases, especially bronchial asthma. For that, articles related to these themes were selected from scientific databases, including human and animal studies. The main findings of this work showed that the respiratory system works as a highly propitious place for the formation of ROS and RNS, especially superoxide anion, hydrogen peroxide, and peroxynitrite, and the epithelial damage is reflected in an important loss of antioxidant defenses that, in turn, culminates in an imbalance and formation of inflammatory and contractile mediators, such as isoprostanes, changes in the activity of protein kinases, and activation of cell proliferation signalling pathways, such as the MAP kinase pathway. Thus, the oxidative imbalance appears as a promising path for future investigations as a therapeutic target for the treatment of asthmatic patients, especially those resistant to currently available therapies.
哮喘是一种气道慢性炎症性疾病,与上皮损伤、对收缩剂的支气管高反应性、组织重塑和管腔狭窄有关。目前,有许多关于哮喘病理生理学的资料;然而,出现了一个新的方面,涉及活性氧和氮物种(ROS 和 RNS)对这种疾病起源的影响。几项研究表明,ROS 和 RNS 的产生与抗氧化酶和非酶系统之间的失衡在这种疾病的发病机制中起着重要作用。考虑到这一方面,本研究旨在从科学文献中收集有关氧化应激在炎症性气道和肺部疾病(特别是支气管哮喘)发展中的作用的数据。为此,从科学数据库中选择了与这些主题相关的文章,包括人类和动物研究。这项工作的主要发现表明,呼吸系统是形成 ROS 和 RNS 的高度有利场所,特别是超氧阴离子、过氧化氢和过氧亚硝酸盐,上皮损伤反映在抗氧化防御的重要损失上,这反过来又导致炎症和收缩性介质的失衡和形成,如异前列腺素、蛋白激酶活性的改变以及细胞增殖信号通路(如 MAP 激酶通路)的激活。因此,氧化失衡似乎是未来作为治疗哮喘患者(特别是对现有治疗方法有抗药性的患者)的治疗靶点的有希望的研究途径。