...
首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Glehnia littoralis Root Extract Inhibits Fat Accumulation in 3T3-L1 Cells and High-Fat Diet-Induced Obese Mice by Downregulating Adipogenic Gene Expression
【24h】

Glehnia littoralis Root Extract Inhibits Fat Accumulation in 3T3-L1 Cells and High-Fat Diet-Induced Obese Mice by Downregulating Adipogenic Gene Expression

机译:Glehnia littoralis根提取物通过下调脂肪基因表达来抑制3T3-L1细胞和高脂饮食诱导的肥胖小鼠的脂肪积累

获取原文
获取原文并翻译 | 示例
           

摘要

Glehnia littoralis has been reported to have several pharmacological properties but no reports describing the antiadipogenic effect of this plant have been published. This study was conducted to investigate the effects of Glehnia littoralis root hot water extract (GLE) and its underlying mechanism on 3T3-L1 cell adipogenesis and in high-fat diet-(HFD-) induced obese mice. We measured intracellular lipid accumulation using oil red Ostaining in vitro. For in vivo study, twenty-eight C57BL/6J male mice were randomly divided into four groups, Control, HFD, HFD+1% GLE, and HFD+5% GLE, which was performed for eight weeks. We determined the expression levels of the adipogenesis-related proteins by RT-PCR and western blotting in HFD-induced obese mice. The GLE dose-dependently inhibited 3T3-L1 adipocyte differentiation and intracellular lipid accumulation in differentiated adipocytes. Further, body weight gain and fat accumulation were significantly lower in the GLE-treated HFD mice than in the untreated HFD mice. GLE treatment suppressed the expression of adipogenic genes such as peroxisome proliferator-activated receptor (PPAR) gamma, CCAAT/enhancer-binding protein (C/EBP) gamma, fatty acid synthase (aP2), and fatty acid synthase (FAS). These results suggest that the GLE inhibits adipocyte differentiation and intracellular lipid accumulation by downregulating the adipogenic gene expression both in vitro and in vivo.
机译:据报道,Glehnia Littoralis有几种药理学特性,但没有报告已经发表了该植物的抗癌原作用。进行该研究以研究Glehnia Littoralis根热水提取物(GLE)的影响及其在3T3-L1细胞脂肪发生和高脂饮食 - (HFD-)诱导的肥胖小鼠上的影响。我们使用氧化油体积体积测量细胞内脂质积累。对于体内研究,将28个C57BL / 6J雄性小鼠随机分为四组,对照,HFD,HFD + 1%GLE和HFD + 5%GLE,其进行八周。我们通过RT-PCR确定了脂肪发生相关蛋白质的表达水平,并在HFD诱导的肥胖小鼠中蛋白质印迹。 GLE剂量依赖性抑制了分化的脂肪细胞中的3T3-L1脂肪细胞分化和细胞内脂质积累。此外,在GLE处理的HFD小鼠中,体重增加和脂肪积聚显着低于未处理的HFD小鼠。 GLE治疗抑制了脂肪生成基因的表达,例如过氧缺血剂增殖剂 - 活化受体(PPAR)γ,CCAAT /增强剂结合蛋白(C / EBP)γ,脂肪酸合酶(AP2)和脂肪酸合酶(FAS)。这些结果表明,通过在体外和体内下调脂肪生成基因表达,GLE抑制脂肪细胞分化和细胞内脂质积累。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号