Department of Nursing, Chang Gung University of Science and Technology, Kwei-Shan, Tao-Yuan, Taiwan, R.O.C.
Mol Nutr Food Res. 2013 Oct;57(10):1803-13. doi: 10.1002/mnfr.201300001. Epub 2013 Jun 17.
Previous studies found that phloretin (PT) and phlorizin (PZ) could inhibit glucose transport, with PT being a better inhibitor of lipid peroxidation. This study aimed to evaluate the antiobesity effects of PT and PZ in 3T3-L1 cells and if they can modulate the relationship between adipocytes and macrophages.
Differentiated 3T3-L1 cells were treated with PT or PZ. Subsequently, transcription factors of adipogenesis and lipolysis proteins were measured. In addition, RAW 264.7 macrophages treated with PT or PZ were cultured in differentiated media from 3T3-L1 cells to analyze inflammatory mediators and signaling pathways. PT significantly enhanced glycerol release and inhibited the adipogenesis-related transcription factors. PT also promoted phosphorylation of AMP-activated protein kinase and increased activity of adipose triglyceride lipase and hormone-sensitive lipase. PT suppressed the nuclear transcription factor kappa-B and mitogen-activated protein kinase pathways when RAW 264.7 cells were cultured in differentiated media from 3T3-L1 cells. PZ improved lipolysis and inhibited the macrophage inflammatory response less effectively than PT.
This study suggests that PT is more effective than PZ at increasing lipolysis in adipocytes. In addition, PT also suppresses inflammatory response in macrophage that is stimulated by differentiated media from 3T3-L1 cells.
先前的研究发现根皮苷(PT)和根皮素(PZ)可以抑制葡萄糖转运,其中 PT 对脂质过氧化的抑制作用更强。本研究旨在评估 PT 和 PZ 在 3T3-L1 细胞中的抗肥胖作用,以及它们是否可以调节脂肪细胞和巨噬细胞之间的关系。
用 PT 或 PZ 处理分化的 3T3-L1 细胞。随后,测量脂肪生成和脂肪分解蛋白的转录因子。此外,用 PT 或 PZ 处理的 RAW 264.7 巨噬细胞在来自 3T3-L1 细胞的分化培养基中培养,以分析炎症介质和信号通路。PT 显著增强了甘油的释放,并抑制了与脂肪生成相关的转录因子。PT 还促进了 AMP 激活蛋白激酶的磷酸化,增加了脂肪甘油三酯脂肪酶和激素敏感脂肪酶的活性。当 RAW 264.7 细胞在来自 3T3-L1 细胞的分化培养基中培养时,PT 抑制了核转录因子 kappa-B 和丝裂原激活蛋白激酶途径。PZ 改善脂肪分解的效果不如 PT ,抑制巨噬细胞炎症反应的效果也不如 PT。
本研究表明,PT 在增加脂肪细胞的脂肪分解方面比 PZ 更有效。此外,PT 还抑制了由 3T3-L1 细胞分化培养基刺激的巨噬细胞的炎症反应。