肥胖症中的炎症微环境和脂肪生成分化:可可碱在体外人肥胖模型中的抑制作用。
Inflammatory Microenvironment and Adipogenic Differentiation in Obesity: The Inhibitory Effect of Theobromine in a Model of Human Obesity In Vitro.
机构信息
Institute of Translational Pharmacology CNR, Via Fosso del Cavaliere, 00133 Rome, Italy.
Department of Systems Medicine, School of Medicine, University of Rome Tor Vergata, Rome, Italy.
出版信息
Mediators Inflamm. 2019 Jan 20;2019:1515621. doi: 10.1155/2019/1515621. eCollection 2019.
OBJECTIVE
Obesity is considered a clinic condition characterized by a state of chronic low-grade inflammation. The role of macrophages and adipocytokines in adipose tissue inflammation is in growing investigation. The physiopathological mechanisms involved in inflammatory state in obesity are not fully understood though the adipocytokines seem to characterize the biochemical link between obesity and inflammation. The aim of this work is to analyze the effect of theobromine, a methylxanthine present in the cocoa, on adipogenesis and on proinflammatory cytokines evaluated in a model of fat tissue inflammation in vitro.
METHODS
In order to mimic in vitro this inflammatory condition, we investigated the interactions between human-like macrophages U937 and human adipocyte cell lines SGBS. The effect of theobromine on in vitro cell growth, cell cycle, adipogenesis, and cytokines release in the supernatants has been evaluated.
RESULTS
Theobromine significantly inhibits the differentiation of preadipocytes in mature adipocytes and reduces the levels of proinflammatory cytokines as MCP-1 and IL-1 in the supernatants obtained by the mature adipocytes and macrophages interaction.
CONCLUSION
Theobromine reduces adipogenesis and proinflammatory cytokines; these data suggest its potential therapeutic effect for treating obesity by control of macrophages infiltration in adipose tissue and inflammation.
目的
肥胖被认为是一种以慢性低度炎症状态为特征的临床病症。巨噬细胞和脂肪细胞因子在脂肪组织炎症中的作用正受到越来越多的研究。尽管脂肪细胞因子似乎是肥胖与炎症之间生化联系的特征,但肥胖炎症状态涉及的生理病理机制尚未完全阐明。本研究旨在分析可可中存在的甲基黄嘌呤可可碱对体外脂肪组织炎症模型中脂肪生成和促炎细胞因子的影响。
方法
为了在体外模拟这种炎症状态,我们研究了类人巨噬细胞 U937 与人脂肪细胞系 SGBS 之间的相互作用。研究了可可碱对体外细胞生长、细胞周期、脂肪生成以及上清液中细胞因子释放的影响。
结果
可可碱可显著抑制前体脂肪细胞向成熟脂肪细胞的分化,并降低成熟脂肪细胞与巨噬细胞相互作用后上清液中促炎细胞因子 MCP-1 和 IL-1 的水平。
结论
可可碱可减少脂肪生成和促炎细胞因子;这些数据表明,可可碱通过控制巨噬细胞浸润脂肪组织和炎症,具有治疗肥胖的潜在治疗效果。