机制(生物学)
体外
药理学
癌症
化学
计算生物学
医学
生物
内科学
生物化学
物理
量子力学
作者
Ning Na,Xiangyang Li,Yi Nan,Guo Qing Chen,Sai Huang,Yuhua Du,Qinxuan Gu,Weiqiang Li,Ling Yuan
出处
期刊:Research Square - Research Square
日期:2024-03-08
标识
DOI:10.21203/rs.3.rs-4002897/v1
摘要
Abstract Aim Network pharmacology combined with cellular experiments to research the mechanism of action of Saikosaponin-d in the treatment of gastric cancer. Methods Drug target genes were obtained from the PubChem database and the Swiss Target Prediction database. Additionally, target genes for gastric cancer were obtained from the GEO database and the Gene Cards database. The core targets were then identified and further analyzed through Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and GESA enrichment. The clinical relevance of the core targets was assessed using the GEPIA database. Molecular docking of drug monomers and core target proteins was performed using Auto Duck Tools and Pymol software. Finally, in vitro cellular experiments including cell viability, apoptosis, cell scratch, Transwell invasion, Transwell migration, qRT-PCR, and Western blot were conducted to verify these findings of network pharmacology. Results The network pharmacology analysis predicted that the drug monomers interacted with 54 disease targets. Based on clinical relevance analysis, six core targets were selected: VEGFA, IL2, CASP3, BCL2L1, MMP2, and MMP1. Molecular docking results showed binding activity between the Saikosaponin-d monomer and these core targets. Conclusion Saikosaponin-d could inhibit gastric cancer cell proliferation, induce apoptosis, and inhibit cell migration and invasion.
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