Nrf2 lowers risk for lung injury induced by diesel exhaust

Diesel exhaust (DE) induced oxidative stress play an important role in proinflammatory reaction on airway. Nrf2 is involved in the transcriptional regulation of many antioxidant genes. In the present study, we investigated the role of Nrf2 in the development of DE induced lung injury in both of Nrf2 +/+ and Nrf2 -/- mice. C57BL/6J Nrf2 +/+ and Nrf2 -/- mice were exposed to DE (DE particle 1mg/m 3 ) or clean air for 8 hrs/day and 6 days/week for 4 weeks. We performed the histopathologic examination of the lung tissues through electron microscope. The cell populations in bronchoalveolar lavage fluid (BALF) and the gene expression of antioxidant enzymes in the lung tissues were examined. An electron microscope study showed the alveolar type II cells injury and degeneration of lamellar body after DE exposure in Nrf2 -/- mice.There were DE particle-laden alveolar macrophages were significantly greater in Nrf2 -/- than in Nrf2 +/+ mice. Neutrophils number in the BALF also significantly increased in Nrf2 -/- mice than in Nrf2 +/+ mice. Expression of antioxidant enzyme genes was significantly increased in Nrf2 +/+ mice after exposed to DE compared with Nrf2 -/- mice. Nrf2 may be an important protective factor against oxidative stresses, and have a possibility to lower the risk for some pulmonary diseases induced by DE.