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吸烟暴露对大鼠肌纤维类型动力学的急性影响。

The acute effects of cigarette smoke exposure on muscle fiber type dynamics in rats.

机构信息

Department of Rehabilitation Sciences, The Hong Kong Polytechnic University, Kowloon, Hong Kong.

Department of Medicine, The University of Hong Kong, Pok Fu Lum, Hong Kong.

出版信息

PLoS One. 2020 May 20;15(5):e0233523. doi: 10.1371/journal.pone.0233523. eCollection 2020.

DOI:10.1371/journal.pone.0233523
PMID:32433675
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7239437/
Abstract

Reduced exercise capacity is common in people with chronic obstructive pulmonary diseases (COPD) and chronic smokers and is suggested to be related to skeletal muscle dysfunction. Previous studies using human muscle biopsies have shown fiber-type shifting in chronic smokers particularly those with COPD. These results, however, are confounded with aging effects because people with COPD tend to be older. In the present study, we implemented an acute 7-day cigarette smoke-exposed model using Sprague-Dawley rats to evaluate early effects of cigarette smoking on soleus muscles. Rats (n = 5 per group) were randomly assigned to either a sham air (SA) or cigarette smoking (CS) groups of three different concentrations of total particulate matters (TPM) (CSTPM2.5, CSTPM5, CSTPM10). Significantly lower percentages of type I and higher type IIa fiber were detected in the soleus muscle in CS groups when compared with SA group. Of these, only CSTMP10 group exhibited significantly lower citrate synthase activity and higher muscle tumor necrosis factor-α level than that of SA group. Tumor necrosis factor-α level was correlated with the percentage of type I and IIa fibers. However, no significant between-group differences were found in fiber cross-sectional area, physical activities, or lung function assessments. In conclusion, acute smoking may directly trigger the onset of glycolytic fiber type shift in skeletal muscle independent of aging.

摘要

运动能力降低在慢性阻塞性肺疾病(COPD)患者和慢性吸烟者中很常见,被认为与骨骼肌功能障碍有关。先前使用人类肌肉活检的研究表明,慢性吸烟者,特别是 COPD 患者,存在纤维类型转变。然而,这些结果与衰老效应相混淆,因为 COPD 患者往往年龄较大。在本研究中,我们使用 Sprague-Dawley 大鼠实施了为期 7 天的急性香烟烟雾暴露模型,以评估吸烟对比目鱼肌的早期影响。大鼠(每组 5 只)随机分为假空气(SA)或香烟烟雾(CS)组,分为三种不同总颗粒物浓度(TPM)(CSTPM2.5、CSTPM5、CSTPM10)。与 SA 组相比,CS 组比目鱼肌中 I 型纤维的百分比明显降低,IIa 型纤维的百分比明显升高。其中,仅 CSTMP10 组的柠檬酸合酶活性明显低于 SA 组,肌肉肿瘤坏死因子-α水平明显高于 SA 组。肿瘤坏死因子-α水平与 I 型和 IIa 型纤维的百分比相关。然而,在纤维横截面积、体力活动或肺功能评估方面,各组之间没有显著差异。总之,急性吸烟可能直接引发骨骼肌糖酵解纤维类型的转变,而与衰老无关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/7239437/eb518c6f6fe8/pone.0233523.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/7239437/e374d9641ab3/pone.0233523.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/7239437/3419c8679235/pone.0233523.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/7239437/bc3efb306d2b/pone.0233523.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/7239437/187d86596b83/pone.0233523.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/7239437/eb518c6f6fe8/pone.0233523.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/7239437/e374d9641ab3/pone.0233523.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/7239437/3419c8679235/pone.0233523.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/7239437/bc3efb306d2b/pone.0233523.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/7239437/187d86596b83/pone.0233523.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/7239437/eb518c6f6fe8/pone.0233523.g005.jpg

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