Beneficial effects of melatonin on stroke-induced muscle atrophy in focal cerebral ischemic rats.
- Author:
Seunghoon LEE
1
;
Jinhee SHIN
;
Yunkyung HONG
;
Minkyung LEE
;
Koo KIM
;
Sang Rae LEE
;
Kyu Tae CHANG
;
Yonggeun HONG
Author Information
- Publication Type:Original Article
- Keywords: Melatonin; muscle atrophy; focal cerebral ischemia
- MeSH: Animals; Fingers; Melatonin; Models, Animal; Muscles; Muscular Atrophy; Myosin Heavy Chains; Phenotype; Protein Isoforms; Rats; RNA, Messenger; Stroke
- From:Laboratory Animal Research 2012;28(1):47-54
- CountryRepublic of Korea
- Language:English
- Abstract: Muscle atrophy is the result of two opposing conditions that can be found in pathological or diseased muscles: an imbalance in protein synthesis and degradation mechanisms. Thus, we investigated whether exogenous melatonin could regulate muscle components in stroke-induced muscle atrophy in rats. Comparing muscle phenotypes, we found that long-term melatonin administration could influence muscle mass. Muscle atrophy-related genes, including muscle atrophy F-box (MAFbx) and muscle ring finger 1 (MuRF1) were significantly down-regulated in melatonin-administered rats in the gastrocnemius. However, only MAFbx at the mRNA level was attenuated in the soleus of melatonin-administered rats. Insulin-like growth factor-1 receptor (IGF-1R) was significantly over-expressed in melatonin-administered rats in both the gastrocnemius and soleus muscles. Comparing myosin heavy chain (MHC) components, in the gastrocnemius, expression of both slow- and fast-type isoforms were significantly enhanced in melatonin-administered rats. These results suggest that long-term exogenous melatonin-administration may have a prophylactic effect on muscle atrophy through the MuRF1/MAFbx signaling pathway, as well as a potential therapeutic effect on muscle atrophy through the IGF-1-mediated hypertrophic signaling pathway in a stroke animal model.
