Nrf2 Is a Protective Factor against Oxidative Stresses Induced by Diesel Exhaust Particle in Allergic AsthmaReportar como inadecuado




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Oxidative Medicine and Cellular LongevityVolume 2013 2013, Article ID 323607, 5 pages

Review Article

Department of Hygiene and Public Health, Graduate School of Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan

Pulmonary Medicine-Infection and Oncology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan

Received 11 January 2013; Revised 18 March 2013; Accepted 8 April 2013

Academic Editor: Hye-Youn Cho

Copyright © 2013 Ying-Ji Li et al.
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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.





Autor: Ying-Ji Li, Tomoyuki Kawada, and Arata Azuma

Fuente: https://www.hindawi.com/



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