基于分子动力学模拟和实验评价探讨黄芪甲苷对HepG2细胞的作用机制

周志朋; 杨明珠; 蔡明钦; 薛娟娣; 吕晓云

doi:10.3971/j.issn.1000-8578.2022.21.1537

基于分子动力学模拟和实验评价探讨黄芪甲苷对HepG2细胞的作用机制

Mechanism of Astragaloside Ⅳ on HepG2 Cells Based on Molecular Dynamics Simulation and Experimental Evaluation

摘要

摘要:
目的基于分子动力学模拟和实验评价揭示黄芪甲苷对HepG2细胞的作用机制。
方法构建“药物-疾病”网络药理图，分析黄芪甲苷（AS-Ⅳ）作用于肝细胞癌（HCC）的核心基因，筛选关键信号通路，建立“药物-靶点”分子动力学模型；体外实验检测HepG2细胞迁移、增殖、侵袭能力；流式细胞术检测HepG2细胞周期及凋亡；qRT-PCR检测核心基因相对表达量。
结果 AS-Ⅳ作用于HCC核心靶点为VEGFA；体外实验结果显示：与对照组比较，高浓度AS-Ⅳ对HepG2细胞的迁移、侵袭和增殖活力具有抑制作用，能阻滞HepG2细胞从G₁期向G₂期转移，促进其凋亡，可下调VEGFA mRNA表达，上调TGF-β1 mRNA表达。
结论 AS-Ⅳ可能通过多靶点、多通路抑制肝癌细胞的增殖。

Abstract:
Objective To reveal the mechanism of action of AS-Ⅳ on HepG2 cells based on molecular dynamics simulation and experimental evaluation.
Methods We constructed a "drug-disease" network pharmacological map, analyzed the core genes of astragaloside Ⅳ (AS-Ⅳ) in HCC, screened key signaling pathways, and established a "drug-target" molecular dynamics model. In vitro assay was used to detect migration, proliferation and invasion abilities. Flow cytometry and qRT-PCR were used to detect the effect of AS-Ⅳ on the cell cycle and apoptosis, and the expression of core gene of HepG2.
Results The core target of AS-Ⅳ acting on HCC was VEGFA. Compared with the control group, the high concentration of AS-Ⅳ significantly inhibited the migration, invasion and proliferation of HepG2 cells, blocked the metastasis of HepG2 cells from G₁ to G₂ phase, promoted their apoptosis, down-regulated VEGFA expression and up-regulated TGF-β1 expression.
Conclusion AS-Ⅳ may inhibit the proliferation of hepatocellular carcinoma cells through multi-target and multi-pathway.

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