基于网络药理学的黄芪-鸡血藤配伍治疗白细胞减少症作用机制研究

目的 采用网络药理学挖掘黄芪-鸡血藤药对配伍治疗白细胞减少症的作用靶点以及信号通路，探究其治疗白细胞减少症的物质基础和作用机制。方法 从TCMSP数据库收集黄芪、鸡血藤的化学活性成分，通过Genecards和CTD数据库收集白细胞减少症的靶点以及所选中药成分作用的靶点。对白细胞减少症疾病靶点以及黄芪-鸡血藤药物靶点进行映射，构建作用靶点的PPI网络模型，筛选出排名前10的Hub基因；采用Cytoscape软件建立化合物-疾病靶点的网络模型，利用DAVID数据库进行GO功能富集分析和KEGG信号通路富集分析。结果 确定黄芪-鸡血藤药对活性化合物治疗白细胞减少症靶点网络包含19个化合物，108个靶点，关键靶点涉及PIK3CA、IL-6、TNF、IL-2、IL-10、KRAS、EGFR、CSF2、IL-3和IL-2RB。涉及的主要KEGG通路富集分析确定信号通路包括细胞因子-细胞因子受体相互作用，药物代谢，造血细胞系，JAK-STAT信号通路等。结论 黄芪-鸡血藤药对是通过调节PIK3CA、IL-6、TNF、IL-2、IL-10等基因，调控药物代谢，细胞因子-细胞因子受体相互作用，造血细胞系，JAK-STAT等信号通路，通过复杂网络模式治疗白细胞减少症。 

Mechanisms of Combination ofAstragali Radix andSpatholobi Caulis in Treatment of Leukopenia Based on Network Pharmacology

OBJECTIVE To investigate the molecular mechanism ofAstragali Radix andSpatholobi Caulis in the treatment of leukopenia by network pharmacology approaches. METHODS The chemical active components ofAstragali Radix andSpatholobi Caulis were collected by Traditional Chinese Medicine Systems Pharmacology （TCMSP） Database， while the target genes for leukopenia and active components were collected by Genecards and CTD databases. The drug targets were mapped to disease targets， the protein-protein interaction network (PPI) of compound-disease was established. The hub genes of the PPI network were screened out. The compound-disease targets network model was visualized by Cytoscape software. Gene Ontology (GO) enrichment and KEGG signaling pathway analysis were generated by DAVID database. RESULTS 19 active components ofAstragali Radix andSpatholobi Caulis， and 108 common targets in treatment of leukopenia were obtained. The core targets were PIK3CA， IL-6， TNF， IL-2， IL-10. KEGG pathway enrichment showed multiple signaling pathways were involved， such as drug metabolism， cytokine-cytokine receptor interaction，hematopoietic cell lineage， JAK-STAT signaling pathway and so on. CONCLUSION The combination application ofAstragali Radix andSpatholobi Caulis in the treatment of leukopenia act on several key targets， such as PIK3CA， IL-6， TNF， IL-2， IL-10， to regulate cytokine-cytokine receptor interaction，drug metabolism， hematopoietic cell lineage and JAK-STAT signaling pathway.