Protective effect of melatonin on TNF-α-induced muscle atrophy in L6 myotubes
- Affiliated Author(s)
- 박재형; 임승순; 송대규; 임정근
- Alternative Author(s)
- Park, Jae Hyung; Im, Seung Soon; Song, Dae Kyu; Lim, Jeong Geun
- Journal Title
- Journal of Pineal Research
- ISSN
- 0742-3098
- Issued Date
- 2013
- Keyword
- antioxidant enzyme activity; L6 myotube; melatonin; muscle atrophy; muscle cell death; reactive oxygen species; TNF-α
- Abstract
- Muscle atrophy, characterized by decreased cell number and size, is a serious concern for patients afflicted with inflammatory diseases. Mounting evidence indicates that tumor necrosis factor alpha (TNF-α) plays a critical role in muscle atrophy in a number of clinical settings. We hypothesize that reactive oxygen species (ROS) mediate TNF-α-induced muscle cell death and hypotrophy. Recently, melatonin has attracted attention because of its free-radical scavenging and antioxidant properties. The aim of the current study was to evaluate the possible protective role of melatonin in TNF-α-induced muscle cell death and hypotrophy in rat L6 myotubes. To examine this possible role, L6 myotubes were exposed to various concentrations of recombinant TNF-α for 24 hr. We found that TNF-α at a concentration of 100 ng/mL induced ROS generation and decreased cell viability. Further analysis revealed that apoptosis, but not autophagy, may be important for TNF-α-induced cell death. Melatonin significantly attenuated TNF-α-induced ROS generation and apoptosis. In addition, decreased muscle fiber diameter and increased muscle cell proteolysis by TNF-α was highly attenuated by treatment with melatonin. The effects of melatonin were mediated neither through its plasmalemmal receptors nor by modulating the nuclear factor kappa B pathway activated by TNF-α. Taken together, these results suggest that TNF-α may mediate ROS-induced muscle cell death and hypotrophy and that melatonin may be a useful tool for protecting against muscle atrophy stemming from inflammatory diseases.
- 공개 및 라이선스
-
- 파일 목록
-
Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.