Artesunate inhibits adipogeneis in 3T3-L1 preadipocytes by reducing the expression and/or phosphorylation levels of C/EBP-α, PPAR-γ, FAS, perilipin A, and STAT-3

被引:41
作者
Jang, Byeong-Churl [1 ]
机构
[1] Keimyung Univ, Coll Med, Dept Mol Med, 1095 Dalgubeoldaero, Daegu 42601, South Korea
基金
新加坡国家研究基金会;
关键词
Artesunate; Adipogenesis; PPAR-gamma; C/EBP-alpha; STAT-3; FAS; ADIPOCYTE DIFFERENTIATION; ADIPOSE-TISSUE; PROTEIN; INSULIN; ADIPONECTIN; OBESITY; LEPTIN; DELTA;
D O I
10.1016/j.bbrc.2016.04.109
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Differentiation of preadipocyte, also called adipogenesis, leads to the phenotype of mature adipocyte. However, excessive adipogenesis is closely linked to the development of obesity. Artesunate, one of artemisinin-type sesquiterpene lactones from Artemisia annua L, is known for anti-malarial and anti-cancerous activities. In this study, we investigated the effect of artesunate on adipogenesis in 3T3-L1 preadipocytes. Artesunate strongly inhibited lipid accumulation and triglyceride (TG) synthesis during the differentiation of 3T3-L1 preadipocytes into adipocytes at 5 mu M concentration. Artesunate at 5 mu M also reduced not only the expressions of CCAAT/enhancer-binding protein-alpha (C/EBP-alpha), peroxisome proliferator-activated receptor-gamma (PPAR-gamma), fatty acid synthase (FAS), and perilipin A but also the phosphorylation levels of signal transducer and activator of transcription-3 (STAT-3) during adipocyte differentiation. Moreover, artesunate at 5 mu M reduced leptin, but not adiponectin, mRNA expression during adipocyte differentiation. Taken together, these findings demonstrate that artesunate inhibits adipogenesis in 3T3-L1 preadipoytes through the reduced expression and/or phosphorylation levels of C/EBP-alpha, PPAR-gamma, FAS, perilipin A, and STAT-3. (C) 2016 Elsevier Inc. All rights reserved.
引用
收藏
页码:220 / 225
页数:6
相关论文
共 32 条
[1]   Adipose tissue as an endocrine organ [J].
Ahima, RS ;
Flier, JS .
TRENDS IN ENDOCRINOLOGY AND METABOLISM, 2000, 11 (08) :327-332
[2]   "Sick Fat," Metabolic Disease, and Atherosclerosis [J].
Bays, Harold E. .
AMERICAN JOURNAL OF MEDICINE, 2009, 122 (01) :S26-S37
[3]   REGULATED EXPRESSION OF 3 C/EBP ISOFORMS DURING ADIPOSE CONVERSION OF 3T3-L1 CELLS [J].
CAO, ZD ;
UMEK, RM ;
MCKNIGHT, SL .
GENES & DEVELOPMENT, 1991, 5 (09) :1538-1552
[4]  
Efferth T, 2001, INT J ONCOL, V18, P767
[5]   Transcriptional control of adipocyte formation [J].
Farmer, Stephen R. .
CELL METABOLISM, 2006, 4 (04) :263-273
[6]   Adipogenesis:: cellular and molecular aspects [J].
Fève, B .
BEST PRACTICE & RESEARCH CLINICAL ENDOCRINOLOGY & METABOLISM, 2005, 19 (04) :483-499
[7]   ESTABLISHED PRE-ADIPOSE CELL LINE AND ITS DIFFERENTIATION IN CULTURE [J].
GREEN, H ;
MEUTH, M .
CELL, 1974, 3 (02) :127-133
[8]   Understanding adipocyte differentiation [J].
Gregoire, FM ;
Smas, CM ;
Sul, HS .
PHYSIOLOGICAL REVIEWS, 1998, 78 (03) :783-809
[9]   Control of energy homeostasis and insulin action by adipocyte hormones: leptin, acylation stimulating protein, and adiponectin [J].
Havel, PJ .
CURRENT OPINION IN LIPIDOLOGY, 2002, 13 (01) :51-59
[10]   Obesity as a medical problem [J].
Kopelman, PG .
NATURE, 2000, 404 (6778) :635-643