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有氧运动可改善衰老大鼠由颗粒物引起的肺部损伤。

Aerobic exercise ameliorates particulate matter-induced lung injury in aging rats.

机构信息

China Institute of Sport Science, Beijing, China; School of Physical Education, Jinan University, Guangzhou, China.

Beijing Research Institute of Sports Science, Beijing, China.

出版信息

Environ Pollut. 2021 Jul 1;280:116889. doi: 10.1016/j.envpol.2021.116889. Epub 2021 Mar 10.

Abstract

Particulate matter 2.5 (PM) is an inflammatory-inducing factor that is considered to be related to many adverse respiratory problems, especially in the elderly. This study aimed to examine whether pre-exercise training could prevent pulmonary injury induced by urban PM in aging rats and investigate its relationship with inflammatory pathways. Male Wistar rats (aged 16 months) were randomly divided into four groups: sedentary, exercise, sedentary + PM exposure, and exercise + PM exposure. All rats in exercise-related groups were treadmill-trained for 8 weeks (65%-75% VO for 30 min every other day). Sedentary groups' rats lived freely in cages without exercise intervention. Rats in the PM-related groups were exposed to ambient PM (4 h day) for 2 weeks after an 8-week exercise intervention or sedentary treatment. Finally, all rats' pulmonary function, lung morphology, degree of inflammation, and relevant protein and mRNA transcript expression levels were examined. The results indicated that PM exposure induced lung injury in the sedentary + PM exposure group, as evidenced by the deterioration of pulmonary function, histopathological characteristics, and inflammatory changes. Aerobic exercise alleviated PM-induced airway obstruction, deterioration of pulmonary function, bronchial mucosal exfoliation, and inflammatory responses in aging rats. These effects in exercise groups were associated with the increased expression of intracellular 70 kDa heat shock protein (iHSP70) and the suppression of nuclear transcription factor-κB (NF-κB) activation, as confirmed by increased expression of inhibitor of NF-κB (IκBα) and a reduction in phospho-IKBα (p-IκBα), which is regulated by inhibiting kappa B kinase beta (IKKβ). Taken together, aerobic pre-exercise had protective effects on lung injury and reduced vulnerability to inflammation induced by PM exposure, possibly through the toll-like receptor 4 (TLR4)/NF-κB signaling pathways mediated by the extracellular-to-intracellular HSP70 ratio. Pre-exercise training may be an effective way to protect against PM-induced lung toxicity in aging individuals.

摘要

颗粒物 2.5(PM)是一种诱导炎症的因素,被认为与许多呼吸道不良问题有关,尤其是在老年人中。本研究旨在探讨运动前训练是否可以预防城市 PM 引起的衰老大鼠肺损伤,并研究其与炎症途径的关系。雄性 Wistar 大鼠(16 月龄)随机分为四组:安静组、运动组、安静+PM 暴露组和运动+PM 暴露组。运动相关组的所有大鼠均进行 8 周的跑步机训练(65%-75%VO,每两天 30 分钟)。安静组的大鼠自由生活在笼子里,没有运动干预。PM 相关组的大鼠在 8 周运动干预或安静处理后进行为期 2 周的环境 PM(4 h/d)暴露。最后,检查所有大鼠的肺功能、肺形态、炎症程度以及相关蛋白和 mRNA 转录表达水平。结果表明,PM 暴露导致安静+PM 暴露组大鼠肺损伤,表现为肺功能恶化、组织病理学特征和炎症变化。有氧运动减轻了 PM 引起的衰老大鼠气道阻塞、肺功能恶化、支气管黏膜脱落和炎症反应。运动组的这些效果与细胞内 70 kDa 热休克蛋白(iHSP70)的表达增加以及核转录因子-κB(NF-κB)激活的抑制有关,这通过抑制κB 激酶β(IKKβ)来调节核因子κB(NF-κB)抑制剂(IκBα)的表达增加和磷酸化 IκBα(p-IκBα)的减少得到证实。综上所述,有氧运动前训练对 PM 暴露引起的肺损伤具有保护作用,并降低了对炎症的易感性,这可能是通过细胞外到细胞内 HSP70 比值介导的 Toll 样受体 4(TLR4)/NF-κB 信号通路。运动前训练可能是预防 PM 引起的老年人肺毒性的有效方法。

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