Huang Wen-Chung, Chen Chi-Yuan, Wu Shu-Ju
1 Graduate Institute of Health Industry Technology, Research Center for Industry of Human Ecology, Research Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology , Taoyuan City, Taiwan .
2 Department of Nutrition and Health Sciences, Research Center for Industry of Human Ecology, Research Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology , Taoyuan City, Taiwan .
J Med Food. 2017 Feb;20(2):103-109. doi: 10.1089/jmf.2016.3806.
Studies have shown that polyphenols reduce the risk of inflammation-related diseases and upregulates energy expenditure in adipose tissue. Here, we investigated the mechanism of the anti-inflammatory and antiobesity effects of almond skin polyphenol extract (ASP) in differentiated 3T3-L1 adipocytes. The antioxidant effects of ASP were measured based on DPPH radical scavenging activity, Trolox equivalent antioxidant capacity, and total phenolic content. Differentiated 3T3-L1 cells were treated with ASP. Subsequently, lipolysis proteins and transcription factors of adipogenesis were measured. The proinflammatory mediators monocyte chemotactic protein-1 (MCP-1) and chemokine ligand 5 (CCL-5) were determined by enzyme-linked immunosorbent assay. We found that ASP significantly promoted phosphorylation of AMP-activated protein kinase (AMPK), increased activity of adipose triglyceride lipase and hormone-sensitive lipase, and inhibited adipogenesis-related transcription factors. In addition, ASP inhibited the tumor necrosis factor-α (TNF-α)-induced cell inflammatory response via downregulation of MCP-1 and CCL-5 secretion. This study suggests that ASP regulates lipolysis through activation of AMPK, reduced adipogenesis, and suppresses proinflammatory cytokines in adipocytes.
研究表明,多酚可降低炎症相关疾病的风险,并上调脂肪组织中的能量消耗。在此,我们研究了杏仁皮多酚提取物(ASP)在分化的3T3-L1脂肪细胞中的抗炎和抗肥胖作用机制。基于DPPH自由基清除活性、Trolox等效抗氧化能力和总酚含量测定了ASP的抗氧化作用。用ASP处理分化的3T3-L1细胞。随后,测量脂肪分解蛋白和脂肪生成的转录因子。通过酶联免疫吸附测定法测定促炎介质单核细胞趋化蛋白-1(MCP-1)和趋化因子配体5(CCL-5)。我们发现,ASP显著促进了AMP活化蛋白激酶(AMPK)的磷酸化,增加了脂肪甘油三酯脂肪酶和激素敏感性脂肪酶的活性,并抑制了脂肪生成相关的转录因子。此外,ASP通过下调MCP-1和CCL-5的分泌来抑制肿瘤坏死因子-α(TNF-α)诱导的细胞炎症反应。这项研究表明,ASP通过激活AMPK来调节脂肪分解,减少脂肪生成,并抑制脂肪细胞中的促炎细胞因子。