Department of Hygiene and Public Health, Graduate School of Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan.
Oxid Med Cell Longev. 2013;2013:323607. doi: 10.1155/2013/323607. Epub 2013 Apr 28.
Epidemiological studies have shown that air pollutants, such as diesel exhaust particle (DEP), are implicated in the increased incidence of allergic airway disorders. In vitro studies of molecular mechanisms have focused on the role of reactive oxygen species generated directly and indirectly by the exposure to DEP. Antioxidants effectively reduce the allergic inflammatory effects induced by DEP both in vitro and in vivo. On the other hand, Nrf2 is a transcription factor essential for the inducible and/or constitutive expression of phase II and antioxidant enzymes. Disruption of Nrf2 enhances susceptibility to airway inflammatory responses and exacerbation of allergic inflammation induced by DEP in mice. Host responses to DEP are regulated by a balance between antioxidants and proinflammatory responses. Nrf2 may be an important protective factor against oxidative stresses induced by DEP in airway inflammation and allergic asthma and is expected to contribute to chemoprevention against DEP health effects in susceptible individuals.
流行病学研究表明,空气污染物,如柴油尾气颗粒(DEP),与过敏性气道疾病发病率的增加有关。体外分子机制研究集中在DEP 直接和间接暴露产生的活性氧的作用。抗氧化剂可有效降低 DEP 在体外和体内引起的过敏性炎症反应。另一方面,Nrf2 是一种转录因子,对于 II 相和抗氧化酶的诱导和/或组成型表达至关重要。Nrf2 的破坏会增加小鼠对气道炎症反应的易感性,并加剧 DEP 引起的过敏性炎症。宿主对DEP 的反应受抗氧化剂和促炎反应之间的平衡调节。Nrf2 可能是对抗DEP 诱导的气道炎症和过敏性哮喘中氧化应激的重要保护因素,并有望有助于预防易感个体的 DEP 健康影响。