Background: Sarcopenia is a complication of chronic obstructive pulmonary disease (COPD) that negatively affects physical activity and quality of life. However, the underlying mechanism by which COPD affects skeletal muscles remains to be elucidated. Therefore, we investigated the association between oxidative stress and structural alterations in muscles of COPD mouse models and verified the effect of astaxanthin on the structural alterations in muscles.
Methods: Twelve-week-old male C57BL/6J mice were treated with intratracheal porcine pancreatic elastase (PPE) dissolved in saline or saline alone. The mice were euthanized 12 weeks after administration, and the lungs and leg muscles were obtained for protein analysis of oxidative stress and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway, muscle atrophy signaling pathway related with oxidative stress. Furthermore, C57BL/6J mice treated with PPE or saline were investigated with the effects of oral administration of astaxanthin.
Results: The weight of the soleus muscle, proportion of type I muscle fibers, and cross-sectional areas of muscle fibers in the COPD mice were lower than those in the control mice. In the mouse model, oxidative stress marker levels were elevated in skeletal muscles. The p38 mitogen-activated protein kinase signaling pathway was activated in the soleus muscles, leading to the activation of the ubiquitin-proteasome system. Astaxanthin attenuated alterations in muscle structure by deactivation of the p38 mitogen-activated protein kinase signaling pathway.
Conclusions: This study provides evidence that oxidative stress induced by COPD triggers a series of muscle structural changes.