首页> 外文期刊>Biomedicine & pharmacotherapy =: Biomedecine & pharmacotherapie >Heshouwu (Polygonum multiflorum Thunb.) ethanol extract suppresses pre-adipocytes differentiation in 3T3-L1 cells and adiposity in obese mice
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Heshouwu (Polygonum multiflorum Thunb.) ethanol extract suppresses pre-adipocytes differentiation in 3T3-L1 cells and adiposity in obese mice

机译:Heshouwu(Polygonum multiflorum thunb。)乙醇萃取液抑制了3T3-L1细胞中的预脂肪细胞分化和肥胖小鼠的肥胖

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摘要

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.
机译:本研究研究了Heshouwu(多糖瘤秋季)的根乙醇提取物(PME)是否具有使用3T3-L1细胞和高脂饮食(HFD)诱导的肥胖小鼠的抗菌活性。用PME(5和10μg/ ml)处理剂量依赖性地抑制了3T3-L1预脂肪细胞分化为脂肪细胞和细胞甘油三酯含量。此外,PME抑制了脂肪生成转录因子的mRNA和蛋白表达,例如CCAAT /增强剂结合蛋白α(C / EBPα)和过氧化物体增殖物激活受体γ(PPARγ),其导致脂肪酸合酶的下调基因表达。与HFD喂养MICE PME(0.05%)12周后,与HFD组相比,它们的内脏脂肪质量,尺寸和体重显着降低。此外,与HFD组相比,PME补充显着上调PPARα,CPT1,CPT2,UCP1和HSL mRNA水平,而其下调PPARγ和DGAT2基因的表达。最后,HFD增加了血清瘦素,胰岛素,葡萄糖和胰岛素和葡萄糖水平;但是,PME扭转了这些变化。这些结果表明,PME可能缓解通过抑制脂肪发生和脂肪生成的肥胖以及通过脂解和脂肪酸氧化在3T3-L1细胞和HFD诱导的肥胖小鼠中。

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