Wang Tao, Yan Ruiqiao, Xu Xiaoyuan, Li Xingnuan, Cao Lingling, Gao Liyun, Liu Jianyun, Zhou Xiaoou, Yu Hui, Wang Xinping, Jiang He, Yang Yaofang
Key Laboratory of System Bio-medicine of Jiangxi Province, Jiujiang University, Jiujiang, 332000, PR China; Department of Pathogenic Biology, School of Basic Medical Sciences, Jiujiang University, Jiujiang, 332000, PR China.
Clinical Skills Center, Clinic Medical College, Jiujiang University, Jiujiang, 332000, PR China.
Acta Histochem. 2019 Feb;121(2):253-259. doi: 10.1016/j.acthis.2018.12.007. Epub 2019 Jan 3.
Understanding the mechanisms of adipogenic differentiation may lead to the discovery of novel therapeutic targets for obesity. The natural plant polyphenol compound curcumin can improve obesity-associated inflammation and diabetes in obese mice. The role of curcumin in adipogenic differentiation of human bone marrow mesenchymal stem cells (hMSCs) is still unclear. We used hMSCs to investigate the details of the mechanism underlying the adipogenic effects of curcumin. At different time points (i.e., 5 days and 10 days) of hMSC adipocyte differentiation, an accumulation of large lipid droplets was analyzed in Oil Red O-stained cultured cells in two curcumin (5 μM and 10 μM) groups and the control group. The cells were also harvested for the detection of mRNA and protein expressions by quantitative real-time polymerase chain reaction and Western blot analysis. The results showed that curcumin can suppresses adipocyte differentiation in a dose-dependent manner and inhibited the expression of PPARγ, C/EBPα, and FABP4. Importantly, curcumin can also suppress the expression of Kruppel-like factor 15, which may bind to the PPARγ promoter, resulting in downregulation of PPARγ expression to inhibit the adipogenic differentiation of hMSCs.
了解脂肪生成分化的机制可能会带来肥胖症新治疗靶点的发现。天然植物多酚化合物姜黄素可改善肥胖小鼠的肥胖相关炎症和糖尿病。姜黄素在人骨髓间充质干细胞（hMSCs）脂肪生成分化中的作用仍不清楚。我们使用hMSCs来研究姜黄素产生脂肪生成作用的潜在机制细节。在hMSC脂肪细胞分化的不同时间点（即5天和10天），分析了两个姜黄素组（5μM和10μM）和对照组中经油红O染色的培养细胞中大量脂滴的积累情况。还通过定量实时聚合酶链反应和蛋白质印迹分析收获细胞以检测mRNA和蛋白质表达。结果表明，姜黄素可剂量依赖性地抑制脂肪细胞分化，并抑制PPARγ、C/EBPα和FABP4的表达。重要的是，姜黄素还可抑制Kruppel样因子15的表达，该因子可能与PPARγ启动子结合，导致PPARγ表达下调，从而抑制hMSCs的脂肪生成分化。
