Life expectancy is increasing worldwide. Lung aging is a process marked by changes in multiple morphological, physiological and age-related biomarkers (e.g., sirtuins) and is influenced by external factors, such as air pollution. Hence, the elderly are considered more vulnerable to the air pollution hazards. We hypothesized that diesel exhaust (DE) exposure intensifies changes in lung inflammatory and structural parameters in aging subjects. Two- and fifteen-month-old mice were exposed to DE for 30 days. Lung function was measured using the forced oscillation method. The inflammatory profile was evaluated in the bronchoalveolar lavage fluid (BALF) and blood, and lung volumes were estimated by stereology. Antioxidant enzyme activity was evaluated by spectrophotometry, sirtuin 1 (SIRT1), sirtuin 2 (SIRT2) and sirtuin 6 (SIRT6) expression was assessed by reverse transcription polymerase chain reaction (RT-PCR), and levels of the sirtuin proteins were evaluated by immunohistochemical staining in lung tissues. Older mice presented decreased pulmonary resistance and elastance, increased macrophage infiltration and decreased tumor necrosis factor (TNF) and interleukin 10 (IL-10) levels in the BALF, reduced activities of the antioxidant enzymes glutathione peroxidase (GPx) and glutathione reductase (GR), and increased activity glutathione S-transferase (GST); increased lung volumes with decreased elastic fiber and increased airway collagen content. SIRT1 gene expression was decreased in older animals, but protein levels were increased. DE exposure increased macrophage infiltration and oxidative stress in the lungs of animals of both ages. SIRT6 gene expression was decreased by DE exposure, with increased protein levels. In older animals, DE affected lung structure and collagen content. Lung aging features, such as decreased antioxidant reserves, lower IL-10 expression, and decreased SIRT1 levels may predispose subjects to exacerbated responses after DE exposure. Our data support the hypothesis that strategies designed to reduce ambient air pollution are an important step towards healthy aging.

世界范围内的预期寿命正在增加。肺衰老是一个以多种形态学，生理学和与年龄有关的生物标志物（例如瑟土因）的变化为标志的过程，并受到诸如空气污染等外部因素的影响。因此，老年人被认为更容易受到空气污染的危害。我们假设柴油机排气（DE）暴露会加剧衰老受试者的肺部炎症和结构参数的变化。将2个月和15个月大的小鼠暴露于DE中30天。使用强制振荡法测量肺功能。在支气管肺泡灌洗液（BALF）和血液中评估炎症状况，并通过体视估计肺容量。抗氧化酶活性通过分光光度法Sirtuin 1（SIRT1）进行评估，通过逆转录聚合酶链反应（RT-PCR）评估sirtuin 2（SIRT2）和sirtuin 6（SIRT6）的表达，并通过免疫组织化学染色在肺组织中评估sirtuin蛋白的水平。老年小鼠的肺阻力和弹性降低，BALF中的巨噬细胞浸润增加，肿瘤坏死因子（TNF）和白介素10（IL-10）水平降低，抗氧化酶谷胱甘肽过氧化物酶（GPx）和谷胱甘肽还原酶（GR）的活性降低。 ，并增加了谷胱甘肽S-转移酶（GST）的活性；肺体积增加，弹性纤维减少，气道胶原含量增加。在年长的动物中，SIRT1基因表达降低，但蛋白质水平升高。暴露于DE会增加两个年龄段动物的肺中巨噬细胞的浸润和氧化应激。暴露于DE会降低SIRT6基因的表达，并增加蛋白质水平。在年长的动物中，DE影响肺的结构和胶原蛋白含量。肺衰老特征，例如抗氧化剂储备降低，IL-10表达降低和SIRT1水平降低，可能使受试者在DE暴露后容易加剧反应。我们的数据支持以下假设：旨在减少环境空气污染的策略是朝着健康衰老迈出的重要一步。降低的SIRT1水平可能会使受试者在DE暴露后容易加剧反应。我们的数据支持以下假设：旨在减少环境空气污染的策略是朝着健康衰老迈出的重要一步。降低的SIRT1水平可能会使受试者在DE暴露后容易加剧反应。我们的数据支持以下假设：旨在减少环境空气污染的策略是朝着健康衰老迈出的重要一步。