王晓昕, 于洪军. 耐力及抗阻训练期间柴油机尾气暴露对小鼠肺部的影响[J]. 体育科学, 2024, 44(3): 51-65. DOI: 10.16469/j.css.202403006
    引用本文: 王晓昕, 于洪军. 耐力及抗阻训练期间柴油机尾气暴露对小鼠肺部的影响[J]. 体育科学, 2024, 44(3): 51-65. DOI: 10.16469/j.css.202403006
    WANG Xiaoxin, YU Hongjun. The Effect of Diesel Engine Exhaust Exposure on the Lungs of Mice during Endurance and Resistance Training[J]. China Sport Science, 2024, 44(3): 51-65. DOI: 10.16469/j.css.202403006
    Citation: WANG Xiaoxin, YU Hongjun. The Effect of Diesel Engine Exhaust Exposure on the Lungs of Mice during Endurance and Resistance Training[J]. China Sport Science, 2024, 44(3): 51-65. DOI: 10.16469/j.css.202403006

    耐力及抗阻训练期间柴油机尾气暴露对小鼠肺部的影响

    The Effect of Diesel Engine Exhaust Exposure on the Lungs of Mice during Endurance and Resistance Training

    • 摘要: 目的:通过观察运动训练和柴油机尾气(diesel engine exhaust,DEE)暴露下肺部指标的变化,探讨不同剂量DEE亚急性暴露期间耐力训练和抗阻训练干预对小鼠肺部反应的综合影响。方法:69只雄性C57BL/6小鼠随机分为9组,分别进行无干预对照或耐力、抗阻训练干预方案,同时将小鼠暴露于过滤、低浓度与中等浓度DEE环境(1 h/d,持续3周)。干预结束后,利用小动物无创全身体积描记法评估小鼠肺功能。收集小鼠肺组织和肺泡灌洗液,通过组织染色观察肺组织结构、纤维化及细胞凋亡情况,采用试剂盒及实时荧光定量聚合酶链式反应(RT-qPCR)评估炎症、氧化应激等指标变化。结果:DEE暴露导致小鼠肺功能下降,肺组织结构发生病理改变,细胞凋亡增加,炎症和氧化应激反应加剧,且这些不良反应随DEE暴露浓度的上升而增加。与暴露对照组相比,DEE暴露同时进行耐力训练和抗阻训练可在一定程度上改善小鼠肺功能,减少肺组织损伤、纤维化和细胞凋亡水平,并伴随丙二醛(malondialdehyde,MDA)含量减少。此外,在中等浓度DEE暴露情况下,抗阻训练组在减轻肺组织损伤,降低乳酸脱氢酶(lactate dehydrogenase,LDH)活性、白细胞介素-6(interleukin-6,IL-6)含量及Ⅲ型胶原蛋白(collagen typeⅢ,Col3a1)、结缔组织生长因子(connective tissue growth factor, Ctgf)、白细胞介素-1β(interleukin-1β,IL-1β)、核因子κB(nuclear factor-kappa B,NF-κB)基因表达水平,提升白细胞介素-10(interleukin-10,IL-10)含量及总超氧化物歧化酶(total superoxide dismutase,T-SOD)、过氧化氢酶(catalase,CAT)活性效果方面优于耐力训练组。值得注意的是,与无污染环境下的不运动小鼠相比,暴露于DEE环境的耐力训练和抗阻训练干预收益效果不会抵消DEE暴露造成的肺部不良反应。结论:运动在一定程度上可以改善DEE引起的肺部损伤,但并不能完全抵消DEE暴露对肺部的负面影响。研究提示了DEE暴露条件下进行运动的潜在益处,但也需要谨慎权衡在实际环境中的应用。

       

      Abstract: Objectives: To investigate the comprehensive effects of endurance training(ET) and resistance training(RT) interventions on the lungs of mice when subacute diesel engine exhaust(DEE) exposure at different doses. Methods: Sixty-nine male C57BL/6 mice were randomly divided into nine groups, they performed either ET or RT intervention except control group; at the same time,the mice were exposed to either filtered air, or low, moderate concentrations of DEE(1 h/d for 3 weeks). The lung function in mice was assessed using whole body plethysmography(WBP). Lung tissues and bronchoalveolar lavage fluid were collected to observe tissue structure, fibrosis, and apoptosis through histological staining. In addition, inflammatory and oxidative stress indicators were evaluated using assay kits and RT-qPCR. Results: The study indicated that DEE exposure led to a decline in lung function, the pathological changes were observed in lung tissue structure, the apoptosis was increased, and inflammatory and oxidative stress responses were intensified. These adverse reactions were found to escalate with the increase of pollutant concentrations. However,the ET and RT interventions during DEE exposure partially ameliorated lung function in mice, including the improvement in lung tissue damage, fibrosis, and apoptosis, accompanied by a decrease in MDA content. Remarkably, under moderate DEE exposure, RT intervention demonstrated superior effects compared with ET in alleviating lung tissue damage, which was evidenced by the reduction in LDH activity, IL-6 level, and Col3a1, Ctgf, IL-1β, NF-κB gene expression, while enhancing IL-10 level and increasing the activities of T-SOD and CAT. It is noteworthy that the exercise intervention under DEE exacerbated adverse lung reactions in mice compared with that of under filtered air. Conclusions: Exercise can mitigate DEE-induced lung injury, but it cannot completely offset all the negative effects of DEE. These findings highlight the potential benefits of exercise under DEE exposure, but the application in practice should be considered carefully.

       

    /

    返回文章
    返回