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首页> 外文期刊>European Journal of Pharmacology: An International Journal >The mechanisms of baicalin ameliorate obesity and hyperlipidemia through a network pharmacology approach
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The mechanisms of baicalin ameliorate obesity and hyperlipidemia through a network pharmacology approach

机译:通过网络药理学方法的黄芩苷改良肥胖和高脂血症的机制

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摘要

Obesity is one of the main causes of human cardiovascular and cerebrovascular diseases. Baicalin, a bioactive flavonoid isolated from the herbal medicine Scutellaria baicalensis Georgi, is reported to ameliorate obesity and hyperlipidemia. However, its mechanism remains unclear. Here, we used network pharmacology to explore the potential mechanism of baicalin on a system level. First, we predicted the targets of baicalin and diseases, and then protein-protein interaction (PPI) networks were constructed. Moreover, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment was performed via the Database for Annotation, Visualization, and Integrated Discovery (DAVID) server. Lastly, we confirmed the results of the network analysis by palmitic acid (PA) treated human hepatoma cells (HepG2) in vitro. The results indicated that 37 targets related to obesity treated by baicalin were predicted by network pharmacology, and top 10 related pathways were extracted by the KEGG database. Baicalin treatment could reduce triglyceride (TG) contents and lipid droplet accumulation in PA-treated HepG2 cells. The anti-obesity effects of baicalin might be due to the up-regulation of solute carrier family 2 member 1 (SLC2A1) and down-regulation of tumor necrosis factor (TNF), nuclear factor kappa B subunit 1 (NFKB1), sterol regulatory element binding transcription factor 1 (SREBF1), peroxisome proliferator activated receptor gamma and caspase 3 (CASP3). Our results indicated that baicalin may regulate key inflammatory markers, adipogenesis process, and apoptosis for treatment of obesity.
机译:肥胖是人类心血管和脑血管疾病的主要原因之一。据报道,来自草药Scutellaria Baicalensis Georgi的生物活性黄酮类生物活性类黄酮,以改善肥胖和高脂血症。但是,它的机制仍然不清楚。在这里,我们使用网络药理学探讨了黄芩苷对系统水平的潜在机制。首先,我们预测了黄芩苷和疾病的目标,然后构建了蛋白质 - 蛋白质相互作用(PPI)网络。此外,通过数据库进行注释,可视化和集成发现(David)服务器,进行基因和基因组(Kegg)途径富集的京都百科全书。最后,我们通过棕榈酸(PA)治疗的人肝癌细胞(HepG2)确认了网络分析的结果。结果表明,通过网络药理学预测了37种与黄芩苷治疗的肥胖症有关的靶标,并通过KEGG数据库提取前10个相关途径。黄芩苷治疗可以将甘油三酯(Tg)含量降低在PA处理的HepG2细胞中的脂质液滴积累。黄芩苷的抗肥胖效果可能是由于溶质载体家族的上调2成员1(SLC2A1)和肿瘤坏死因子(TNF),核因子κB亚基1(NFKB1)下调,固醇调节元件结合转录因子1(SreBF1),过氧化物体增殖剂活化受体γ和胱天蛋白酶3(Casp3)。我们的研究结果表明,黄芩苷可以调节关键的炎症标志物,脂肪发生过程和治疗肥胖症的凋亡。

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