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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Soshiho-Tang Aqueous Extract Exerts Antiobesity Effects in High Fat Diet-Fed Mice and Inhibits Adipogenesis in 3T3-L1 Adipocytes
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Soshiho-Tang Aqueous Extract Exerts Antiobesity Effects in High Fat Diet-Fed Mice and Inhibits Adipogenesis in 3T3-L1 Adipocytes

机译:Soshiho-Tang含水提取物在高脂饮食喂食小鼠中施加抗菌作用,并抑制3T3-L1脂肪细胞的脂肪组织

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摘要

Soshiho-tang (SST; sho-saiko-to in Japanese; xiaochaihu-tang in Chinese) has generally been used to improve liver fibrosis-and cirrhosis-related symptoms in traditional Korean medicine. Although many studies have investigated the pharmacological properties of SST, its antiobesity effect has not been elucidated. Thus, our present study was carried out to evaluate the antiobesity effect of SST using a high fat diet- (HFD) induced obese mouse model and 3T3-L1 adipose cells. C57BL/6J mice were randomly divided into four groups (n = 6/group), normal diet (ND), HFD-fed group, and HFD- and SST-fed groups (S200: 200 mg/kg of SST; S600: 600 mg/kg of SST) and given HFD with or without SST extract for 8 weeks. 3T3-L1 preadipocytes were differentiated into adipocytes for 8 days with or without SST. In the HFD-fed obese mice, body weight and fat accumulation in adipose tissue were significantly reduced by SST administration. Compared with control-differentiated adipocytes, SST significantly inhibited lipid accumulation by decreasing the triglyceride (TG) content and leptin concentration in 3T3-L1 adipocytes. SST also decreased the expression of adipogenesis-related genes including lipoprotein lipase (LPL), fatty acid binding protein 4 (FABP4), CCAAT/enhancer-binding protein-alpha (C/EBP-a), and peroxisome proliferator-activated receptor-gamma (PPAR-gamma). Our findings suggest that SST has potential as a nontoxic antiobesity medication.
机译:Soshiho-Tang(SST; SHO-SAIKO-TO in Japanese;中文中的小译,Xiachaihu-Tang一般用于改善传统韩国医学中的肝纤维化和肝硬化相关的症状。虽然许多研究已经研究了SST的药理学性质,但尚未阐明其抗菌作用。因此,我们本研究进行了使用高脂饮食(HFD)诱导的肥胖小鼠模型和3T3-L1脂肪细胞来评估SST的抗血液效应。将C57BL / 6J小鼠随机分为四组(n = 6 /组),正常饮食(Nd),HFD喂料组和HFD-和SST-FED组(S200:200 mg / kg SST; S600:600 Mg / kg SST)和给定或没有SST提取物的HFD 8周。将3T3-L1前脂肪细胞与或不含SST分化为脂肪细胞8天。在HFD喂养的肥胖小鼠中,SST给药显着降低了脂肪组织中的体重和脂肪积累。与对照分化的脂肪细胞相比,SST通过降低3T3-L1脂肪细胞中的甘油三酯(Tg)含量和瘦素浓度而显着抑制脂质积累。 SST还降低了脂肪生成相关基因的表达,包括脂蛋白脂肪酶(LPL),脂肪酸结合蛋白4(FABP4),CCAAT /增强剂结合蛋白-α(C / EBP-A)和过氧化物组增殖物激活受体-γ (PPAR-GAMMA)。我们的研究结果表明,SST具有潜在的无毒抗菌药物。

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