Qin Fei, Fan Zhengzheng, Xu Minxiao, Wang Zhongwei, Dong Yanan, Qu Chaoyi, Cui Shuqiang, Zhao Lina, Zhao Jiexiu
Sport Biological Center, China Institute of Sport Science, Beijing, China.
School of Physical Education, Jinan University, Guangzhou, China.
Front Physiol. 2021 Oct 26;12:731594. doi: 10.3389/fphys.2021.731594. eCollection 2021.
Ambient particulate matter (PM), as an inflammation-inducing factor, increases the prevalence of lung injury. The aim of this study was to examine the protective effect and mechanism of aerobic exercise on PM exposure-induced lung injury. Forty Wistar rats were randomly divided into four groups: sedentary+PM exposure, exercise+PM exposure, sedentary, and exercise groups. All rats in the exercise-related groups underwent 8-week aerobic interval treadmill training (5daysweek, 1hday). PM-exposed rats were exposed to ambient PM (6h day) for 3weeks after the 8-week exercise intervention. Then, ventilation function, histopathological changes, and inflammation responses of pulmonary tissue were examined. Results showed that PM exposure induced lung injury as manifested by decreased pulmonary function, abnormal histopathological changes, and increased pro-inflammatory cytokine levels (tumor necrosis factor-α and Interleukin-1α). Aerobic exercise alleviated the airway obstruction, reduced respiratory muscle strength, bronchial mucosal exfoliation, ultrastructure damage, and inflammatory responses induced by PM in exercise-related groups. The benefits of exercise were related with the downregulation of p38-mitogen-activated protein kinase (MAPK), and the subsequent inhibition of the pathways of the cyclooxygenase 2 (COX-2) product, prostaglandin E (PGE). Thus, pre-exercise training may be an effective way to protect against PM-induced lung inflammatory injury in rats.
环境颗粒物（PM）作为一种炎症诱导因子，会增加肺损伤的发生率。本研究的目的是探讨有氧运动对PM暴露所致肺损伤的保护作用及机制。将40只Wistar大鼠随机分为四组：久坐+PM暴露组、运动+PM暴露组、久坐组和运动组。运动相关组的所有大鼠均接受为期8周的有氧间歇跑步机训练（每周5天，每天1小时）。在进行8周的运动干预后，PM暴露组大鼠每天暴露于环境PM（6小时）3周。然后，检测肺组织的通气功能、组织病理学变化和炎症反应。结果表明，PM暴露可导致肺损伤，表现为肺功能下降、组织病理学变化异常以及促炎细胞因子水平升高（肿瘤坏死因子-α和白细胞介素-1α）。有氧运动减轻了运动相关组中PM诱导的气道阻塞、呼吸肌力量减弱、支气管黏膜剥脱、超微结构损伤和炎症反应。运动的益处与p38丝裂原活化蛋白激酶（MAPK）的下调以及随后对环氧化酶2（COX-2）产物前列腺素E（PGE）途径的抑制有关。因此，运动预训练可能是预防大鼠PM诱导的肺部炎症损伤的有效方法。
