Inhibition of adipogenesis by Tempol in 3T3-L1 cells.
Inhibition of adipogenesis by Tempol in 3T3-L1 cells.
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DOI：
10.1016/j.freeradbiomed.2010.05.028
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发表时间：
2010-08-15
影响因子：
7.4
通讯作者：
Mitchell, James B.
中科院分区：
文献类型：
--
作者：
Samuni, Yuval;Cook, John A.;Choudhuri, Rajani;DeGraff, William;Sowers, Anastasia L.;Krishna, Murali C.;Mitchell, James B.
肥胖与包括高血压、心血管疾病、糖尿病和癌症在内的严重健康状况的风险增加高度相关。随着氧化应激的增加，氧化还原状态的变化与肥胖有关。先前的研究表明，在小鼠的食物中加入抗氧化剂Tempol可以防止肥胖，导致体重显著减轻，而没有毒性。为了更好地理解这种作用的分子机制，研究了Tempol对小鼠3 T3-L1前脂肪细胞分化的影响。Tempol可抑制3 T3-L1细胞的分化，导致细胞脂质储存减少，关键脂肪形成转录因子（PPAR-γ和PPAR-α）的蛋白水平下调，脯氨酰羟化酶下调，HIF-1α上调。Tempol饮食的小鼠显示出降低的IGF-1全身水平，与体外在3 T3-L1细胞中观察到的定性一致，3 T3-L1细胞也显示出较低的IGF-1水平作为Tempol治疗的结果。这些结果表明，用Tempol处理3 T3-L1细胞抑制关键脂肪形成因子的表达、脂肪分化和脂质储存，并且可能至少部分地是Tempol对体重的一些体内作用的基础。
Obesity is highly associated with an increased risk of serious health conditions including hypertension, cardiovascular disease, diabetes, and cancer. Changes in redox status with increased oxidative stress have been linked with obesity. Previous studies have shown that administration of the antioxidant Tempol in the food of mice prevents obesity causing significant weight loss without toxicity. To gain a better understanding of the molecular mechanism(s) underlying this effect, the influence of Tempol on the differentiation of mouse 3T3-L1 pre-adipocytes was studied. Tempol inhibited differentiation of 3T3-L1 cells resulting in a reduction in cellular lipid storage, down-regulation of protein levels of key adipogenesis transcription factors (PPAR-γ and PPAR-α), down regulation of prolyl hydroxylase, and up-regulation of HIF-1α. Mice on a Tempol diet demonstrated reduced systemic levels of IGF-1, in qualitative agreement with that observed in vitro in 3T3-L1 cells, which also show lower IGF-1 levels as a result of Tempol treatment. These results show that treatment of 3T3-L1 cells with Tempol inhibits the expression of key adipogenesis factors, adipose differentiation, and lipid storage and may underlie, at least in part, some of the in vivo effects of Tempol on body weight.
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