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- Title
Doxorubicin inhibits muscle inflammation after eccentric exercise.
- Authors
Huang, Sheng ‐ Chih; Wu, Jin ‐ Fu; Saovieng, Suchada; Chien, Wei ‐ Horng; Hsu, Ming ‐ Fen; Li, Xiao ‐ Fei; Lee, Shin ‐ Da; Huang, Chih ‐ Yang; Kuo, Chia ‐ Hua
- Abstract
Background Doxorubicin, a widely used anti-tumour drug, is known to cause muscle loss in cancer patients. Methods Following an acute dose of doxorubicin injection (2.5 mg/kg per body weight), we examined macrophage distribution in rat soleus muscle challenged by eccentric exercise (downhill running). Long-term doxorubicin treatment (one injection every 3 days) on muscle mass and survival were also determined. Results Under non-exercised condition, increased tumour necrosis factor (TNF)-alpha mRNA and decreased IL-10 mRNA were observed in soleus muscle of doxorubicin-treated rats, compared with saline-treated control rats. However, increases in inflammation score (leukocyte infiltration), nitrotyrosine level, and M1 macrophage (CD68+) invasion in exercised soleus muscle were absent in doxorubicin-treated rats, whereas increased M2 macrophage (CD163+) localization in exercised muscle was less affected by doxorubicin. Despites coenzyme Q (Q10) supplementation significantly elevated TNF-alpha mRNA, nitrotyrosine, and anti-oxidant gamma-glutamylcysteine synthetase (GCS) levels in non-exercised soleus muscle, these pro-inflammatory responses were also abolished in doxorubicin-treated rats. Results from long-term doxorubicin treatment show a significant muscle loss followed by an accelerated death, which cannot be reversed by Q10 supplementation. Conclusions (i) Doxorubicin impairs inflammation mechanism by depleting M1 macrophage in exercised skeletal muscle; (ii) Muscle loss and accelerated death during prolonged doxorubicin treatment cannot be reversed by Q10 supplementation.
- Subjects
DOXORUBICIN; CANCER patients; MACROPHAGES; NITROTYROSINE; SKELETAL muscle
- Publication
Journal of Cachexia, Sarcopenia & Muscle, 2017, Vol 8, Issue 2, p277
- ISSN
2190-5991
- Publication type
Article
- DOI
10.1002/jcsm.12148