香烟暴露递增诱导 COPD 骨骼肌功能障碍大鼠模型：一项初步研究。
The rat model of COPD skeletal muscle dysfunction induced by progressive cigarette smoke exposure: a pilot study.
机构信息
Department of Sports Medicine, Shanghai University of Sport, Shanghai, 200438, China.
School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
出版信息
BMC Pulm Med. 2020 Mar 23;20(1):74. doi: 10.1186/s12890-020-1109-y.
BACKGROUND
Chronic obstructive pulmonary disease (COPD) skeletal muscle dysfunction is a prevalent malady that significantly affects patients' prognosis and quality of life. Although the study of this disease has attracted considerable attention, a definite animal model is yet to be established. This study investigates whether smoke exposure could lead to the development of a COPD skeletal muscle dysfunction model in rats.
METHODS
Sprague Dawley rats were randomly divided into model (MG, n = 8) and control groups (CG, n = 6). The MG was exposed to cigarette smoke for 16 weeks while the CG was not. The body weight and forelimb grip strength of rats were monitored monthly. The pulmonary function and the strength of tibialis anterior muscle were assessed in vitro and compared after establishing the model. The histological changes in lung and gastrocnemius muscles were observed. The expressions of interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α were detected by ELISA, while the expressions of Atrogin-1 and MuRF1 in the gastrocnemius muscle were determined by Western blotting.
RESULTS
Smoke exposure slowly increases the body weight and forelimb grip strength of MG rats, compared to CG rats. However, it significantly decreases the pulmonary ventilation function and the skeletal muscle contractility of the MG in vitro. Histologically, the lung tissues of MG show typical pathological manifestations of emphysema, while the skeletal muscles present muscular atrophy. The expressions of IL-6, IL-8, and TNF-α in MG rats are significantly higher than those measured in CG rats. Increased levels of Atrogin-1 and MuRF1 were also detected in the gastrocnemius muscle tissue of MG.
CONCLUSION
Progressive smoking exposure decreases the contractile function of skeletal muscles, leading to muscular atrophy. It also increases the expressions of inflammatory and muscle protein degradation factors in COPD rats. This indicates that smoke exposure could be used to establish a COPD skeletal muscle dysfunction model in rats.
背景
慢性阻塞性肺疾病（COPD）骨骼肌功能障碍是一种普遍存在的疾病，严重影响患者的预后和生活质量。尽管对这种疾病的研究已经引起了相当多的关注，但尚未建立明确的动物模型。本研究探讨了吸烟是否会导致大鼠 COPD 骨骼肌功能障碍模型的发展。
方法
将 Sprague Dawley 大鼠随机分为模型组（MG，n=8）和对照组（CG，n=6）。MG 暴露于香烟烟雾中 16 周，而 CG 不暴露。每月监测大鼠的体重和前肢握力。建立模型后，在体外评估肺功能和胫骨前肌强度，并进行比较。观察肺和比目鱼肌的组织学变化。通过 ELISA 检测白细胞介素（IL）-6、IL-8 和肿瘤坏死因子（TNF）-α的表达，通过 Western blot 检测比目鱼肌中 Atrogin-1 和 MuRF1 的表达。
结果
与 CG 大鼠相比，烟雾暴露会缓慢增加 MG 大鼠的体重和前肢握力。然而，它显著降低了 MG 大鼠的肺通气功能和体外骨骼肌收缩力。组织学上，MG 肺组织显示典型的肺气肿病理表现，而骨骼肌表现为肌肉萎缩。MG 大鼠的 IL-6、IL-8 和 TNF-α表达明显高于 CG 大鼠。还检测到 MG 大鼠比目鱼肌组织中 Atrogin-1 和 MuRF1 的水平升高。
结论
逐渐吸烟暴露降低了骨骼肌的收缩功能，导致肌肉萎缩。它还增加了 COPD 大鼠中炎症和肌肉蛋白降解因子的表达。这表明吸烟暴露可用于建立大鼠 COPD 骨骼肌功能障碍模型。
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