Li Ying-Ji, Shimizu Takako, Shinkai Yusuke, Hirata Yukiyo, Inagaki Hirofumi, Takeda Ken, Azuma Arata, Yamamoto Masayuki, Kawada Tomoyuki
Department of Hygiene and Public Health, Nippon Medical School, Tokyo 113-0031, Japan.
The Center for Environmental Health Science for the Next Generation, Research Institute for Science and Technology, Tokyo University of Science, Noda 278-8510, Japan.
Int J Mol Sci. 2017 Mar 17;18(3):649. doi: 10.3390/ijms18030649.
The present study investigated the effects of diesel exhaust (DE) on an experimental model of bleomycin (BLM)-induced lung injury and fibrosis in mice. BLM was intravenously administered to both and C57BL/6J mice on day 0. The mice were exposed to DE for 56 days from 28 days before the BLM injection to 28 days after the BLM injection. Inhalation of DE induced significant inhibition of airway clearance function and the proinflammatory cytokine secretion in macrophages, an increase in neutrophils, and severe lung inflammatory injury, which were greater in mice than in mice. In contrast, inhalation of DE was observed to induce a greater increase of hydroxyproline content in the lung tissues and significantly higher pulmonary antioxidant enzyme mRNA expression in the mice than in mice. DE is an important risk factor, and Nrf2 regulates the risk of a DE inhalation induced immune response during BLM lung injury and fibrosis in mice.
本研究调查了柴油废气（DE）对博来霉素（BLM）诱导的小鼠肺损伤和纤维化实验模型的影响。在第0天，对野生型和C57BL/6J小鼠均静脉注射BLM。从BLM注射前28天至BLM注射后28天，将小鼠暴露于DE中56天。吸入DE可显著抑制气道清除功能和巨噬细胞中促炎细胞因子的分泌，增加中性粒细胞数量，并导致严重的肺部炎症损伤，野生型小鼠的这些损伤比C57BL/6J小鼠更严重。相比之下，观察到吸入DE可使野生型小鼠肺组织中羟脯氨酸含量增加更多，且肺抗氧化酶mRNA表达显著高于C57BL/6J小鼠。DE是一个重要的风险因素，并且Nrf2调节小鼠在BLM肺损伤和纤维化过程中吸入DE诱导的免疫反应风险。
