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Anti-adipogenic effects of viscothionin in 3T3-L1 adipocytes and high fat diet induced obesity mice
Applied Biological Chemistry ( IF 2.3 ) Pub Date : 2020-02-05 , DOI: 10.1186/s13765-020-0489-2
Sokho Kim , Seo-Hyun Ahn , Jong-Heum Park , Chan Hum Park , Yu Su Sin , Gee-Wook Shin , Jungkee Kwon

Viscum album subsp. Coloratum, also known as Korean mistletoe, is a traditional herb that has more recently been used for the treatment of nervine, hypertensive and cardiovascular diseases. Therefore, this study was undertaken to access the anti-obesity effect of Korean mistletoe-derived polypeptide viscothionin using 3T3-L1 adipocytes in vitro and in vivo mouse experimental model. Viscothionin (up to 5 μM) was used to treat mouse 3T3-L1 pre-adipocytes during adipocyte differentiation. Adipocyte differentiation in 3T3-L1 cells was confirmed by Oil Red O staining. Obesity was induced by a high-fat diet (HFD) in C57BL/6J mice, followed by oral administration of viscothionin (up to 10 mg/kg) for 3 weeks. As a result, viscothionin (5 μM) inhibited differentiation of adipocyte cells and attenuated accumulation of intracellular lipids through activation of 5′-adenosine monophosphate-activated protein kinase (AMPK), by down-regulating phosphorylation in AKT and glycogen synthase kinase 3β (GSK3β). Treatment of viscothionin also decreased the levels of sterol regulatory element binding protein-1 (SREBP-1) and its target gene, fatty acid synthase (FAS). Moreover, viscothionin (10 mg/kg) significantly suppressed body weight and fat content, and improved serum lipid concentration, compared with the standard drug simvastatin (10 mg/kg), a well-known anti-obesity agent. The present study suggests, that viscothionin exerts anti-adipogenic effect through the activation of AMPK and has potential to prevent HFD-induced obesity.

中文翻译:

粘硫蛋白对3T3-L1脂肪细胞和高脂饮食诱导的肥胖小鼠的抗脂肪形成作用

Viscum相册子版本。Coloratum,也被称为韩国槲寄生,是一种传统草药,最近已用于治疗神经,高血压和心血管疾病。因此,本研究旨在利用3T3-L1脂肪细胞在体外和体内小鼠实验模型中获得韩国槲寄生衍生的多肽粘硫蛋白的抗肥胖作用。在脂肪细胞分化过程中,使用粘蛋白(最高5μM)处理小鼠3T3-L1前脂肪细胞。通过油红O染色证实了3T3-L1细胞中的脂肪细胞分化。在C57BL / 6J小鼠中,通过高脂饮食(HFD)诱导肥胖,然后口服粘连性硫黄素(最高10 mg / kg)3周。结果是,通过下调AKT和糖原合酶激酶3β(GSK3β)的磷酸化,粘硫蛋白(5μM)通过激活5'-腺苷单磷酸激活的蛋白激酶(AMPK)抑制脂肪细胞的分化并减少细胞内脂质的积累。粘连蛋白的治疗还降低了固醇调节元件结合蛋白1(SREBP-1)及其靶基因脂肪酸合酶(FAS)的水平。此外,与众所周知的抗肥胖药标准药物辛伐他汀(10毫克/千克)相比,粘连蛋白(10毫克/千克)显着抑制了体重和脂肪含量,并改善了血脂浓度。本研究表明,粘连蛋白通过激活AMPK发挥抗脂肪形成作用,并具有预防HFD诱发肥胖的潜力。
更新日期:2020-02-05
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