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The Inhibitory Effects of Juglanin on Adipogenesis in 3T3-L1 Adipocytes
Drug Design, Development and Therapy ( IF 4.7 ) Pub Date : 2020-12-02 , DOI: 10.2147/dddt.s256504
Guang Wang 1 , Bing Wu 2 , Wenzhou Xu 3 , Xuefei Jin 4 , Kun Wang 5 , Heyuan Wang 6
Affiliation  

Introduction: Deregulation of adipogenesis plays an important role in obesity and other metabolism disorders. PPAR, C/EBP and SREBP1c are key transcriptional factors involved in adipogenesis and lipogenesis. Juglanin is a natural compound belonging to flavonoids, and it has been reported that juglanin has a potent inhibitory effect on inflammation and certain type of cancers. However, the effects of juglanin in adipogenesis have not been reported before.
Materials and Methods: 3T3-L1 preadipocytes were incubated with differentiation induction medium in the presence or absence of 0.5, 2.5, or 5 μM juglanin for an 8-day differentiation period. The lipid droplets accumulated in the cytoplasm were monitored by Oil Red O staining on days 0, 2, 5, and 8. The regulatory effects of juglanin on adipogenesis-related genes and proteins were investigated by real-time polymerase chain reaction and Western blot analysis.
Results: Juglanin significantly decreased lipid accumulation in differentiated adipocytes. Our findings show that juglanin reduced the expression of C/EBPα, C/EBPβ, and SREBP-1c without affecting PPARα or PPARγ expression. Additionally, juglanin increased the activation of the SIRT1/AMPK signaling pathway through the phosphorylation of AMPKα. Finally, we performed an AMPK inhibitor experiment, which revealed that the inhibitory effects of juglanin on adipogenesis are mediated through AMPK.
Discussion: Juglanin can prevent adipogenesis by suppressing lipid accumulation and the differentiation of preadipocytes. The mechanism of juglanin regulating adipogenesis requires further investigation. Future clinical study in vivo could shed more light on its implication in modulating obesity and metabolic disorders.

Keywords: Juglanin, adipogenesis, obesity, lipid metabolism, AMPK


中文翻译:


胡桃素对3T3-L1脂肪细胞脂肪生成的抑制作用



简介:脂肪生成失调在肥胖和其他代谢紊乱中起着重要作用。 PPAR、C/EBP 和 SREBP1c 是参与脂肪生成和脂肪生成的关键转录因子。胡桃素是一种天然化合物,属于黄酮类化合物,据报道,胡桃素对炎症和某些类型的癌症具有有效的抑制作用。然而,胡桃素对脂肪形成的影响此前尚未有报道。

材料和方法:在存在或不存在 0.5、2.5 或 5 μM 胡桃素的情况下,将 3T3-L1 前脂肪细胞与分化诱导培养基一起孵育 8 天的分化期。在第0、2、5和8天通过油红O染色监测细胞质中积累的脂滴。通过实时聚合酶链反应和蛋白质印迹分析研究胡桃素对脂肪生成相关基因和蛋白质的调节作用。

结果:胡桃素显着降低分化脂肪细胞中的脂质积累。我们的研究结果表明,胡桃素降低了 C/EBPα、C/EBPβ 和 SREBP-1c 的表达,而不影响 PPARα 或 PPARγ 的表达。此外,胡桃素通过 AMPKα 磷酸化增加 SIRT1/AMPK 信号通路的激活。最后,我们进行了 AMPK 抑制剂实验,结果表明胡桃素对脂肪生成的抑制作用是通过 AMPK 介导的。

讨论:胡桃素可以通过抑制脂质积累和前脂肪细胞的分化来防止脂肪形成。胡桃素调节脂肪生成的机制需要进一步研究。未来的体内临床研究可以进一步阐明其在调节肥胖和代谢紊乱方面的意义。


关键词:胡桃素, 脂肪生成, 肥胖, 脂质代谢, AMPK
更新日期:2020-12-02
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