Heshouwu (Polygonum multiflorum Thunb.) ethanol extract suppresses pre-adipocytes differentiation in 3T3-L1 cells and adiposity in obese mice
Heshouwu (Polygonum multiflorum Thunb.) ethanol extract suppresses pre-adipocytes differentiation in 3T3-L1 cells and adiposity in obese mice
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DOI：
10.1016/j.biopha.2018.06.140
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发表时间：
2018-10-01
影响因子：
7.5
通讯作者：
Lee, Mi-Kyung
中科院分区：
文献类型：
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作者：
Choi, Ra-Yeong;Lee, Hae-In;Lee, Mi-Kyung
本研究调查了何首乌（Polygonum multiflorum Thunb.）根乙醇提取物（PME）使用3 T3-L1细胞和高脂饮食（HFD）诱导的肥胖小鼠具有抗肥胖活性。PME（5和10 μ g/mL）处理剂量依赖性地抑制3 T3-L1前脂肪细胞分化为脂肪细胞和细胞甘油三酯含量。此外，PME抑制成脂转录因子如CCAAT/增强子结合蛋白α（C/EBP α）和过氧化物酶体增殖物激活受体γ（PPAR γ）的mRNA和蛋白质表达，从而导致脂肪酸合成酶基因表达下调。用HFD喂养小鼠PME（0.05%）12周后，与HFD组相比，小鼠的内脏脂肪量、大小和体重均显着减少。此外，与HFD组相比，PME补充显著上调了PPAR α、CPT 1、CPT 2、UCP 1和HSL mRNA水平，而下调了PPAR γ和DGAT 2基因的表达。最后，HFD增加血清瘦素，胰岛素，葡萄糖和胰岛素和葡萄糖水平，然而，PME逆转这些变化。这些结果表明，PME可能通过抑制3 T3-L1细胞和HFD诱导的肥胖小鼠中的脂肪生成和脂肪生成以及通过脂解和脂肪酸氧化来减轻肥胖。
This study investigated whether Heshouwu (Polygonum multiflorum Thunb.) root ethanol extract (PME) has antiobesity activity using 3T3-L1 cells and high-fat diet (HFD)-induced obese mice. Treatment with PME (5 and 10 mu g/mL) dose-dependently suppressed 3T3-L1 pre-adipocyte differentiation to adipocytes and cellular triglyceride contents. In addition, PME inhibited mRNA and protein expression of adipogenic transcription factors such as CCAAT/enhancer-binding protein alpha (C/EBP alpha) and peroxisome proliferator-activated receptor gamma (PPAR gamma), which led to down-regulation of fatty acid synthase gene expression. After feeding mice PME (0.05%) with HFD for 12 weeks, their visceral fat mass, size and body weight were significantly reduced compared with the HFD group. Furthermore, PME supplementation significantly up-regulated the PPAR alpha, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPAR gamma and DGAT2 genes. Finally, HFD increased serum leptin, insulin, glucose and insulin and glucose levels; however, PME reversed these changes. These results demonstrated that PME might relieve obesity that occurs via inhibition of adipogenesis and lipogenesis as well as through lipolysis and fatty acid oxidation in 3T3-L1 cells and HFD-induced obese mice.