The rat model of COPD skeletal muscle dysfunction induced by progressive cigarette smoke exposure: a pilot study

Su, Jianqing; Li, Jian; Lu, Yufan; Li, Ning; Li, Peijun; Wang, Zhengrong; Wu, Wenqing; Liu, Xiaodan

doi:10.1186/s12890-020-1109-y

Cited by 13 publications

(17 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 42 Another group reported that 16-week exposure of male Sprague-Dawley rats to cigarette smoke leads to less contractility of tibialis anterior muscles and a reduced cross-sectional area of gastrocnemius muscles, as well as emphysematous changes in the lung, elevated inflammatory factors in the serum, and ubiquitin protease induction in muscle tissue. 43 Additionally, in the present study, we showed a reduction in muscle mass and sMyHC-positive fibers in the smoke-exposed mice. Considering these data, rodents exposed to cigarette smoke for several months represent a well-established model for sarcopenia with COPD.…”

Section: Discussionsupporting

confidence: 70%

<p>Ninjin’yoeito Ameliorates Skeletal Muscle Complications in COPD Model Mice by Upregulating Peroxisome Proliferator-Activated Receptor γ Coactivator-1α Expression</p>

Miyamoto¹,

Asai²,

Kadotani³

et al. 2020

COPD

View full text Add to dashboard Cite

Purpose: Sarcopenia, the loss of skeletal muscle mass and strength, is a common systemic consequence of chronic obstructive pulmonary disease (COPD) and is correlated with higher mortality. Ninjin'yoeito (NYT) is a Japanese herbal medicine used to treat athrepsia and anorexia and is reported to ameliorate weight loss and muscular dysfunction. Recent studies have shown that its crude components upregulate the peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α)-related pathway, which is involved in skeletal muscle functions. Here, we examined whether NYT improves skeletal muscle complications by upregulating PGC-1α in COPD model mice. Materials and Methods: Mice were divided into four groups: control, NYT, smoking, and smoking + NYT. The smoking and smoking + NYT groups were exposed to cigarette smoke for 60 min once daily. The mice in the NYT and smoking + NYT groups were fed an NYT-containing diet (3% w/w). We performed cellular analysis of bronchoalveolar lavage fluid, assessed pulmonary morphological changes, examined the expression of PGC-1α mRNA and protein in the gastrocnemius and soleus muscle, measured the hindlimb muscle volume with micro-computed tomography, and determined the myofiber proportion in soleus muscle after 12 weeks. Results: Cigarette smoke exposure resulted in reduced skeletal muscle volume and slowtwitch muscle fibers and development of pulmonary emphysema. NYT feeding induced partial recovery of the damaged alveolar wall; however, NYT did not ameliorate smokeinduced alveolar enlargement. These findings revealed that NYT did not have sufficient efficacy in suppressing pulmonary emphysema. On the other hand, PGC-1α expression in muscle tissue of the NYT-fed mice increased significantly, resulting in suppression of smokeinduced loss of muscle mass and alteration in the muscle fiber distribution. Conclusion: NYT increases PGC-1α expression in the muscle of COPD model mice and is involved in suppressing cigarette smoke-induced muscle complications. NYT may be a novel preventive and therapeutic medication for muscular dysfunctions in COPD.

show abstract

Section: Discussionsupporting

confidence: 70%

<p>Ninjin’yoeito Ameliorates Skeletal Muscle Complications in COPD Model Mice by Upregulating Peroxisome Proliferator-Activated Receptor γ Coactivator-1α Expression</p>

Miyamoto¹,

Asai²,

Kadotani³

et al. 2020

COPD

View full text Add to dashboard Cite

show abstract

“…Consistent with previous studies showing MuRF-1 up-regulation in the skeletal muscles of CSexposed animals, CS exposure tended to increase MuRF-1 in WT mice (Figure 6). 11,39,40 Additionally, the markedly enhanced MuRF-1 protein levels in CS-exposed Parkin À/À mice further support the notion that Parkin plays a pivotal role in negatively regulating MuRF-1 protein levels in muscles during CS exposure. The participation of MuRF-1 in the process of MHC degradation was confirmed through MuRF-1 knockdown experiments, which showed significant recovery from CSE-induced MHC reduction in the myotubes (Figure 4).…”

Section: Discussionsupporting

confidence: 66%

Involvement of Parkin‐mediated mitophagy in the pathogenesis of chronic obstructive pulmonary disease‐related sarcopenia

Ito

Hashimoto

Tanihata

et al. 2022

J cachexia sarcopenia muscle

View full text Add to dashboard Cite

Background Sarcopenia is characterized by the loss of skeletal muscle mass and strength and is associated with poor prognosis in patients with chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) exposure, a major cause for COPD, induces mitochondrial damage, which has been implicated in sarcopenia pathogenesis. The current study sought to examine the involvement of insufficient Parkin-mediated mitophagy, a mitochondrion-selective autophagy, in the mechanisms by which dysfunctional mitochondria accumulate with excessive reactive oxygen species (ROS) production in the development of COPD-related sarcopenia. Methods The involvement of Parkin-mediated mitophagy was examined using in vitro models of myotube formation, in vivo CS-exposure model using Parkin À/À mice, and human muscle samples from patients with COPD-related sarcopenia. Results Cigarette smoke extract (CSE) induced myotube atrophy with concomitant 30% reduction in Parkin expression levels (P < 0.05). Parkin-mediated mitophagy regulated myotube atrophy by modulating mitochondrial damage and mitochondrial ROS production. Increased mitochondrial ROS was responsible for myotube atrophy by activating Muscle Ring Finger 1 (MuRF-1)-mediated myosin heavy chain (MHC) degradation. Parkin À/À mice with prolonged CS exposure showed enhanced limb muscle atrophy with a 31.7% reduction in limb muscle weights (P < 0.01) and 2.3 times greater MuRF-1 expression (P < 0.01) compared with wild-type mice with concomitant accumulation of damaged mitochondria and oxidative modifications in 4HNE expression. Patients with COPD-related sarcopenia exhibited significantly reduced Parkin but increased MuRF-1 protein levels (35% lower and 2.5 times greater protein levels compared with control patients, P < 0.01 and P < 0.05, respectively) and damaged mitochondria accumulation demonstrated in muscles. Electric pulse stimulation-induced muscle contraction prevented CSE-induced MHC reduction by maintaining Parkin levels in myotubes. Conclusions Taken together, COPD-related sarcopenia can be attributed to insufficient Parkin-mediated mitophagy and increased mitochondrial ROS causing enhanced muscle atrophy through MuRF-1 activation, which may be at least partly preventable through optimal physical exercise.

show abstract

“…Chronic obstructive pulmonary disease (COPD) is a chronic, debilitating disease, predominantly induced by air pollution and aging (Su et al, 2020). It is a major cause of chronic morbidity and the third leading cause of death globally (World Health Organization, 2018).…”

mentioning

confidence: 99%

Association between Sleep Duration and Hand Grip Strength among COPD Patients

Wang

Chen

et al. 2021

West J Nurs Res

View full text Add to dashboard Cite

This study aimed to evaluate the association between night-time sleep duration and hand grip strength (HGS) among patients with chronic obstructive pulmonary disease (COPD). Participants aged ≥45 years were included in a nationally representative investigation clinical study in 2015. HGS was measured using dynamometers. The data on night-time sleep duration, sociodemographic information, and health-related variables were systematically collected. For analysis, sleep duration was categorized as <5 h, 5–7 h, 7 h, 7–9 h, and >9 h. Multivariable linear regression models were used to determine the possible association between the night-time sleep duration and HGS. Our results indicated that the shortest (<5 h) or the longest sleep duration (>9 h) was relevant to high risk of weaker HGS in females. In males, the shortest (<5 h) sleep duration was correlated to lower HGS. Thus, our findings clearly suggest that health care providers should focus on the potential influence of sleep duration on HGS among COPD patients.

show abstract

The rat model of COPD skeletal muscle dysfunction induced by progressive cigarette smoke exposure: a pilot study

Cited by 13 publications

References 51 publications

<p>Ninjin’yoeito Ameliorates Skeletal Muscle Complications in COPD Model Mice by Upregulating Peroxisome Proliferator-Activated Receptor γ Coactivator-1α Expression</p>

<p>Ninjin’yoeito Ameliorates Skeletal Muscle Complications in COPD Model Mice by Upregulating Peroxisome Proliferator-Activated Receptor γ Coactivator-1α Expression</p>

Involvement of Parkin‐mediated mitophagy in the pathogenesis of chronic obstructive pulmonary disease‐related sarcopenia

Association between Sleep Duration and Hand Grip Strength among COPD Patients

Contact Info

Product

Resources

About