散血明目片治疗视网膜静脉阻塞的作用机制探析:基于网络药理学

Based on Network Pharmacology to Explore the Mechanism of Sanxue Mingmu Tablet in the Treatment of Retinal Vein Occlusion

目的:基于网络药理学方法探讨散血明目片治疗视网膜静脉阻塞的作用机制。方法:通过中药系统药理学数据库(TCMSP)获得散血明目片的主要化学成分,通过DrugBank、Online Mendelian Inheritancein Man Database(OMIM)、Pharmacogenetics and Pharmacogenomics Knowledge Base(PharmGKB)搜集视网膜静脉阻塞的疾病靶点,结合Cytoscape 3.8.0软件构建药物-核心靶点-有效成分网络、靶标蛋白互作(PPI)网络,并利用Bioconductor中的R包对核心靶点进行基因本体论(GO)富集和京都基因与基因组百科(KEGG)通路分析,研究其作用机制。结果:获得活性成分77个,药物靶点1 544个,获得疾病靶点625个,获得交集基因17个。通过PPI蛋白作用网络分析,核心蛋白涉及VEGFA、KDR、CYP3A4、ABCG2、MYC等。GO富集到了1 234个GO条目。通过KEGG通路富集分析,发现主要涉及化学致癌作用-受体激活通路、EGFR酪氨酸激酶抑制通路、MAPK信号通路、PI3K-Akt信号通路等。结论:散血明目片的主要成分通过化学致癌作用-受体激活通路、EGFR酪氨酸激酶抑制通路、MAPK信号通路、PI3K-Akt信号通路等信号通路作用于VEGFA、KDR、CYP3A4、ABCG2、MYC治疗视网膜静脉阻塞。

Objective:To explore the mechanism of Sanxue Mingmu tablet in the treatment of retinal vein occlusion based on network pharmacology.Methods:The main chemical constituents of Sanxue Mingmu tablets were obtained by using DrugBank,Online Mendelian-Inheritancein Man Database(OMIM),Pharmacogenetics and Pharmacogenetics Pharmacogenomics Knowledge Disease targets of retinal vein occlusion were collected by Base(PharmGKB),and drug-core-target-active component network and target protein interaction(PPI)network were constructed with Cytoscape 3.8.0software.Gene ontology(GO)enrichment and Kyoto gene were performed on core targets using R package in Bioconductor And genome Encyclopedia(KEGG)pathway analysis to study its mechanism.Results:77active ingredi-ents,1544drug targets,625disease targets and 17overlapping genes were obtained.PPI protein network analysis showed that the core proteins involved VEGFA,KDR,CYP3A4,ABCG2,MYC and so on.GO enriched to 1234GO items.KEGG pathway enrichment analysis found that chemical carcinogenesis-receptor activation pathway,EGFR tyrosine kinase inhibition pathway,MAPK signaling pathway,PI3K-Akt signaling pathway and other signaling path-ways.Conclusion:The main components of Sanxue Mingmu tablets act on VEGFA,KDR,CYP3A4,ABCG2and MYC through chemical carcinogenic receptor activation pathway,EGFR tyrosine kinase inhibition pathway,MAPK signaling pathway,PI3K-Akt signaling pathway and other signaling pathways.