Acute Exposure to Diesel-Biodiesel Particulate Matter Promotes Murine Lung Oxidative Stress by Nrf2/HO-1 and Inflammation Through the NF-kB/TNF- Pathways
Acute Exposure to Diesel-Biodiesel Particulate Matter Promotes Murine Lung Oxidative Stress by Nrf2/HO-1 and Inflammation Through the NF-kB/TNF- Pathways
复制标题
DOI：
10.1007/s10753-018-0910-8
复制
发表时间：
2019-04-01
期刊：
影响因子：
5.1
通讯作者：
Romana-Souza, Bruna
中科院分区：
文献类型：
--
作者：
Cattani-Cavalieri, Isabella;Valenca, Samuel Santos;Romana-Souza, Bruna
燃料燃烧造成的空气污染会造成呼吸障碍，从而可能导致死亡。我们的目的是研究生物柴油（DB）燃烧对小鼠肺的影响。从一辆公共汽车发动机的排气管中收集DB颗粒物。小鼠连续5天鼻内滴注250 g或1000 g DB颗粒物。我们证明了DB颗粒物在250 g和1000 g组中穿透肺。此外，与对照小鼠相比，250 g组肺实质中的DB颗粒物数量高175倍，1000 g组高300倍。滴注DB颗粒物增加了小鼠肺中的巨噬细胞数量和TNF-α的蛋白水平。与对照组相比，DB颗粒物增强了两个暴露组的ROS产生和丙二醛水平。与对照组和250 g组相比，250 g组的Nrf 2、p-NF-kB和HO-1蛋白表达水平较高，1000 g组较低。总之，DB颗粒物滴注通过激活Nrf 2/HO-1促进氧化应激，通过p-NF-kB/TNF-α途径促进炎症。
Air pollution caused by fuel burning contributes to respiratory impairments that may lead to death. We aimed to investigate the effects of biodiesel (DB) burning in mouse lungs. DB particulate matter was collected from the exhaust pipes of a bus engine. Mice were treated with 250g or 1000g of DB particulate matter by intranasal instillation over 5 consecutive days. We demonstrated that DB particulate matter penetrated the lung in the 250-g and 1000-g groups. In addition, the DB particulate matter number in pulmonary parenchyma was 175-fold higher in the 250-g group and 300-fold higher in the 1000-g group compared to control mice. The instillation of DB particulate matter increased the macrophage number and protein levels of TNF-alpha in murine lungs. DB particulate matter enhanced ROS production in both exposed groups and the malondialdehyde levels compared to the control group. The protein expression levels of Nrf2, p-NF-kB, and HO-1 were higher in the 250-g group and lower in the 1000-g group than in control mice and the 250-g group. In conclusion, DB particulate matter instillation promotes oxidative stress by activating the Nrf2/HO-1 and inflammation by p-NF-kB/TNF-alpha pathways.