論文 - 詳細
| RRC ID | 61628 |
|---|---|
| 著者 | Li YJ, Shimizu T, Shinkai Y, Ihara T, Sugamata M, Kato K, Kobayashi M, Hirata Y, Inagaki H, Uzuki M, Akimoto T, Umezawa M, Takeda K, Azuma A, Yamamoto M, Kawada T. |
| タイトル | Nrf2 Lowers the Risk of Lung Injury via Modulating the Airway Innate Immune Response Induced by Diesel Exhaust in Mice. |
| ジャーナル | Biomedicines |
| Abstract |
In the present study, we investigated the role of Nrf2 in airway immune responses induced by diesel exhaust (DE) inhalation in mice. C57BL/6J Nrf2+/+ and Nrf2-/- mice were exposed to DE or clean air for 8 h/day and 6 days/week for 4 weeks. After DE exposure, the number of neutrophils and macrophage inflammatory protein (MIP)-2 level in bronchoalveolar lavage fluid (BALF) and interleukin (IL)-17 level in the lung tissue increased in Nrf2-/- mice compared with Nrf2+/+ mice; however, the lack of an increase in the level of tumor necrosis factor (TNF)-α in the lung tissue in Nrf2+/+ mice and mild suppression of the level of TNF-α in Nrf2-/- mice were observed; the level of granulocyte macrophage colony-stimulating factor (GM-CSF) in the lung tissue decreased in Nrf2-/- mice than in Nrf2+/+ mice; the number of DE particle-laden alveolar macrophages in BALF were larger in Nrf2-/- mice than in Nrf2+/+ mice. The results of electron microscope observations showed alveolar type II cell injury and degeneration of the lamellar body after DE exposure in Nrf2-/- mice. Antioxidant enzyme NAD(P)H quinone dehydrogenase (NQO)1 mRNA expression level was higher in Nrf2+/+ mice than in Nrf2-/- mice after DE exposure. Our results suggested that Nrf2 reduces the risk of pulmonary disease via modulating the airway innate immune response caused by DE in mice. |
| 巻・号 | 8(10) |
| 公開日 | 2020-10-21 |
| DOI | 10.3390/biomedicines8100443 |
| PII | biomedicines8100443 |
| PMID | 33096811 |
| PMC | PMC7589508 |
| IF | 4.717 |
| リソース情報 | |
| 実験動物マウス | RBRC01390 |