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运动通过调节抗氧化基因和金属蛋白酶预防香烟烟雾引起的膈肌废用。

Exercise Prevents Diaphragm Wasting Induced by Cigarette Smoke through Modulation of Antioxidant Genes and Metalloproteinases.

机构信息

Physical Therapy Division, University of Brasília and Department of Physical Therapy, Universidade Paulista, Brasília, DF, Brazil.

Department of Medicine (LIM 20), School of Medicine, University of Sao Paulo, Sao Paulo, SP, Brazil.

出版信息

Biomed Res Int. 2018 Mar 29;2018:5909053. doi: 10.1155/2018/5909053. eCollection 2018.

DOI:10.1155/2018/5909053
PMID:29789801
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5896353/
Abstract

BACKGROUND

The present study aimed to analyze the effects of physical training on an antioxidant canonical pathway and metalloproteinases activity in diaphragm muscle in a model of cigarette smoke-induced chronic obstructive pulmonary disease (COPD).

METHODS

Male mice were randomized into control, smoke, exercise, and exercise + smoke groups, which were maintained in trial period of 24 weeks. Gene expression of kelch-like ECH-associated protein 1; nuclear factor erythroid-2 like 2; and heme-oxygenase1 by polymerase chain reaction was performed. Metalloproteinases 2 and 9 activities were analyzed by zymography. Exercise capacity was evaluated by treadmill exercise test before and after the protocol.

RESULTS

Aerobic training inhibited diaphragm muscle wasting induced by cigarette smoke exposure. This inhibition was associated with improved aerobic capacity in those animals that were submitted to 24 weeks of aerobic training, when compared to the control and smoke groups, which were not submitted to training. The aerobic training also downregulated the increase of matrix metalloproteinases (MMP-2 and MMP-9) and upregulated antioxidant genes, such as nuclear factor erythroid-2 like 2 (NRF2) and heme-oxygenase1 (HMOX1), in exercise + smoke group compared to smoke group.

CONCLUSIONS

Treadmill aerobic training protects diaphragm muscle wasting induced by cigarette smoke exposure involving upregulation of antioxidant genes and downregulation of matrix metalloproteinases.

摘要

背景

本研究旨在分析在香烟烟雾诱导的慢性阻塞性肺疾病(COPD)模型中,体育锻炼对抗氧化经典途径和膈肌金属蛋白酶活性的影响。

方法

雄性小鼠被随机分为对照组、吸烟组、运动组和运动+吸烟组,在 24 周的试验期内保持。通过聚合酶链反应进行 Kelch 样 ECH 相关蛋白 1;核因子红细胞 2 样 2;血红素加氧酶 1 的基因表达。通过酶谱法分析金属蛋白酶 2 和 9 的活性。在方案前后通过跑步机运动试验评估运动能力。

结果

有氧运动训练抑制了香烟烟雾暴露引起的膈肌肌肉萎缩。与未接受训练的对照组和吸烟组相比,这种抑制与经过 24 周有氧运动训练的动物的有氧能力提高有关。有氧运动训练还下调了基质金属蛋白酶(MMP-2 和 MMP-9)的增加,并上调了抗氧化基因,如核因子红细胞 2 样 2(NRF2)和血红素加氧酶 1(HMOX1),在运动+吸烟组与吸烟组相比。

结论

跑步机有氧运动训练可防止香烟烟雾暴露引起的膈肌肌肉萎缩,涉及抗氧化基因的上调和基质金属蛋白酶的下调。

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