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人参皂苷F2通过与过氧化物酶体增殖物激活受体γ(PPARγ)结合并抑制3T3-L1细胞系中的脂肪细胞分化而具有抗肥胖活性。

Ginsenoside F2 possesses anti-obesity activity via binding with PPARγ and inhibiting adipocyte differentiation in the 3T3-L1 cell line.

作者信息

Siraj Fayeza Md, SathishKumar Natarajan, Kim Yeon Ju, Kim Se Young, Yang Deok Chun

机构信息

Korean Ginseng Center and Ginseng Resource Bank, Kyung Hee University , Yongin , Korea.

出版信息

J Enzyme Inhib Med Chem. 2015 Feb;30(1):9-14. doi: 10.3109/14756366.2013.871006. Epub 2014 Mar 25.

Abstract

Abstract Panax ginseng Meyer has been shown to be effective in mitigating various diseases. Protopanaxadiols (PPD) and protopanaxatriols (PPT), which are the main constituents of ginseng, have been shown to impact obesity. Therefore, we selected several important ginsenosides to perform our docking study and determine if they had binding affinity with the peroxisome proliferator activated receptor gamma (PPARγ), which is a major transcription factor in adipocytes. Among them, only a few ginsenosides demonstrated binding affinity with PPARγ. Other than ginsenoside F2 rest of them were previously reported by the researchers in experimental study in case of obesity cell line 3T3-L1 adipocyte. In few recent studies, it was reported that F2 has protective effects on malignant brain tumors as well as anti-cancer activity in breast cancer. Therefore, we felt it was important to focus on F2 when considering obesity. Our study focused on this ginsenoside and analyzed its impact on 3T3-L1 adipocytes. Following the molecular interaction studies, further experimental studies were carried out and demonstrated that ginsenoside F2 when treated with different doses reduces the level of lipid accumulated by the 3T3-L1 cell line during adipogenesis. Reverse transcriptase polymerase chain reaction (RT-PCR) and quantitative real-time PCR results showed reduction in PPARγ and perilipin gene expression levels compared to that of differentiated adipocytes without any treatment. So considering the binding with a major adipocyte transcription factor and the performed experiments, we suggest that ginsenoside F2 may reduce obesity via the inhibition of adipogenesis in the 3T3-L1 cell line.

摘要

摘要 人参已被证明对减轻多种疾病有效。人参的主要成分原人参二醇(PPD)和原人参三醇(PPT)已被证明会影响肥胖。因此,我们选择了几种重要的人参皂苷进行对接研究,以确定它们是否与过氧化物酶体增殖物激活受体γ(PPARγ)具有结合亲和力,PPARγ是脂肪细胞中的一种主要转录因子。其中,只有少数人参皂苷显示出与PPARγ的结合亲和力。除了人参皂苷F2外,其他几种人参皂苷在肥胖细胞系3T3-L1脂肪细胞的实验研究中已有研究人员报道。最近的一些研究报道,F2对恶性脑肿瘤具有保护作用,对乳腺癌也有抗癌活性。因此,我们认为在考虑肥胖问题时关注F2很重要。我们的研究聚焦于这种人参皂苷,并分析了它对3T3-L1脂肪细胞的影响。在进行分子相互作用研究之后,又开展了进一步的实验研究,结果表明,用不同剂量处理的人参皂苷F2可降低3T3-L1细胞系在脂肪生成过程中积累的脂质水平。逆转录聚合酶链反应(RT-PCR)和定量实时PCR结果显示,与未经任何处理的分化脂肪细胞相比,PPARγ和脂滴包被蛋白基因的表达水平有所降低。因此,考虑到与主要脂肪细胞转录因子的结合以及所进行的实验,我们认为人参皂苷F2可能通过抑制3T3-L1细胞系的脂肪生成来减轻肥胖。

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