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首页> 外文期刊>Oxidative Medicine and Cellular Longevity >Network Pharmacology Analysis and Molecular Characterization of the Herbal Medicine Formulation Qi-Fu-Yin for the Inhibition of the Neuroinflammatory Biomarker iNOS in Microglial BV-2 Cells: Implication for the Treatment of Alzheimer’s Disease
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Network Pharmacology Analysis and Molecular Characterization of the Herbal Medicine Formulation Qi-Fu-Yin for the Inhibition of the Neuroinflammatory Biomarker iNOS in Microglial BV-2 Cells: Implication for the Treatment of Alzheimer’s Disease

机译：中药制剂的网络药理学分析及分子表征齐富粘抑制小胶质增生BV-2细胞中神经炎性生物标志物Inos的抑制作用：对阿尔茨海默病治疗的影响

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Aberrant microglial activation drives neuroinflammation and neurodegeneration in Alzheimer’s disease (AD). The present study is aimed at investigating whether the herbal formula Qi-Fu-Yin (QFY) could inhibit the inflammatory activation of cultured BV-2 microglia. A network pharmacology approach was employed to predict the active compounds of QFY, protein targets, and affected pathways. The representative pathways and molecular functions of the targets were analyzed by Gene Ontology (GO) and pathway enrichment. A total of 145 active compounds were selected from seven herbal ingredients of QFY. Targets (e.g., MAPT, APP, ACHE, iNOS, and COX-2) were predicted for the selected active compounds based on the relevance to AD and inflammation. As a validation, fractions were sequentially prepared by aqueous extraction, ethanolic precipitation, and HPLC separation, and assayed for downregulating two key proinflammatory biomarkers iNOS and COX-2 in lipopolysaccharide- (LPS-) challenged BV-2 cells by the Western blotting technique. Moreover, the compounds of QFY in 90% ethanol downregulated iNOS in BV-2 cells but showed no activity against COX-2 induction. Among the herbal ingredients of QFY, Angelicae Sinensis Radix and Ginseng Radix et Rhizoma contributed to the selective inhibition of iNOS induction. Furthermore, chemical analysis identified ginsenosides, especially Rg3, as antineuroinflammatory compounds. The herbal formula QFY may ameliorate neuroinflammation via downregulating iNOS in microglia.
机译：异常的小胶质激活驱动阿尔茨海默病（AD）的神经炎性和神经变性。本研究旨在研究草药齐富尹（QFY）是否可以抑制培养的BV-2小胶质细胞的炎症活化。使用网络药理学方法来预测QFY，蛋白质靶标和受影响途径的活性化合物。通过基因本体（GO）和途径富集分析靶标的代表性途径和分子函数。共选出145个活性化合物，选自七种QFY的草药成分。基于与AD和炎症的相关性，预测所选活性化合物的靶标（例如MAPT，APP，ACHE，INOS和COX-2）。作为验证，通过萃取水溶液，乙醇沉淀和HPLC分离顺序制备级分，并测定通过Western印迹技术在脂多糖 - （LPS-）挑战的BV-2细胞中下测量两个关键促炎生物标志物Inos和Cox-2。此外，QFY在90％乙醇中的QFY化合物在BV-2细胞中下调INOS，但没有针对COX-2诱导的活性。在QFY的草药成分中，Angelicae Sinensis Radix和Ginseng Natix等rhizoma有助于选择性抑制Inos诱导。此外，化学分析确定了人参皂苷，特别是RG3，作为抗肿瘤炎炎症化合物。草药QFY可以通过在微胶质细胞中下调INOS来改善神经炎炎症。

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