Protective Effect of Melatonin against TNF-α Toxicity in the L6 Muscle Cell Line

Other Titles
L6 근육 세포주에서의 TNF-α 독성에 대한 멜라토닌의 보호 효과
Authors
정은지
Issue Date
2011-12
Awarded Date
2012
Abstract
Muscle atrophy poses a serious concern to patients inflicted with inflammatory muscle diseases. An increasing body of evidence implies that tumor necrosis factor-α (TNF-α) plays a critical role in muscle atrophy in a number of these clinical settings. We hypothesize that reactive oxygen species (ROS) mediate TNF-α-induced muscle cell death and muscle atrophy. Recently, melatonin has attracted attention because of its free radical scavenging and antioxidant properties. The aim of this study was to evaluate the possible role of melatonin in preventing TNF-α-induced cell death in rat L6 myocytes. To examine the functional significance and detailed morphological characteristics of TNF-α-induced muscle proteolysis, L6 myocytes were subjected to increasing concentrations of recombinant TNF-α for 24 and 48 hours. TNF-α at a concentration of 100 ng/ml induced ROS generation and decreased the viability. Further analysis of cell death showed that TNF-α-induced apoptosis. Melatonin significantly attenuated TNF-α-induced apoptosis.. Melatonin inhibited TNF-α-induced apoptosis by scavenging ROS through decreasing mitochondrial metabolism and increasing cellular antioxidant enzyme activity in TNF-α-treated L6 myotubes. Taken together, these results suggest that ROS might be, at least partially, mediated in TNF-α-induced muscle proteolysis and melatonin may be useful as an agents preventing muscle atrophy associated with inflammatory diseases.
근위축은 염증성 근육질환을 겪고 있는 환자들에게 심각한 문제를 야기한다. 특히, 염증성 사이토카인인 TNF-α가 근위축에서 중요한 역할을 한다는 많은 보고가 있다. TNF-α에 의해 발생한 활성 산소가 근육 세포의 사멸과 근위축을 유도할 것이라는 가정하에 본 연구를 진행하였다. 최근에 멜라토닌은 자유 라티칼 제거 및 항산화 효과가 알려지면서 큰 관심을 받게되었다. 본 연구에서는 L6 근육세포주에서 TNF-α에 의한 세포사멸에 대한 멜라토닌의 보호제로서의 가능성을 알아보았다. TNF-α에 의해 근육 단백 분해의 자세한 분자적 특성을 알아보기 위해 분화된 L6 근육세포에 TNF-α를 24시간 동안 농도별로 처리해보았다. 100 ng/mL TNF-α에 의해 활성 산소가 세포내에 발생하였고, 또한 세포의 사멸을 유도하였다. 멜라토닌은 세포 내 미토콘드리아 대사율을 감소시키고, 항산화 효소 활성도를 증가시켜 세포내 활성산소를 제거함으로써 TNF-α에 의한 세포사멸을 억제하였다. 이상의 결과로 보아 멜라토닌은 염증성 근육질환과 관련된 근위축 치료에 도움이 될 수 있을 것이다.
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/11549
Appears in Collections:
3. 학위논문 > 1. School of Medicine (의과대학) > 박사
Full Text
http://dcollection.kmu.ac.kr//jsp/common/DcLoOrgPer.jsp?sItemId=000000010338
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