基于网络药理学探究黄芪白术药对治疗骨质疏松性骨折的作用机制

目的:基于网络药理学探讨黄芪白术药对治疗骨质疏松性骨折(osteoporotic fracture, OPF)的潜在作用机制。方法:应用中药系统药理学数据库及分析平台(TCMSP)筛选黄芪、白术的活性成分及作用靶点,检索与疾病靶点有关的GeneCards、OMIM、TTD数据库筛选OPF的作用靶点,进而筛选黄芪、白术与OPF的交集核心靶点,并运用Cytoscape 3.7.1软件构建化合物靶点疾病网络,基于DAVID数据库对靶点进行GO功能富集和KEGG通路富集分析。结果:基于TCMSP数据库筛选黄芪白术治疗OPF的活性成分19个和交集靶点115个；GO功能富集分析得到条目568个,其中生物过程条目433个、细胞组成条目43个、分子功能条目92个；KEGG通路富集分析得出条目111个,主要包括糖尿病并发症中的AGE-RAGE、IL-17、TNF、前列腺癌、Toll样受体、HIF-1、NF-κB等信号通路。结论:黄芪白术药对可能通过调控TNF、NF-κB、HIF-1等信号通路,发挥调控炎症反应以及破骨细胞和成骨细胞的内在平衡作用,从而对OPF产生治疗作用。

Network pharmacology of Astragalus membranaceus-Atractylodes macrocephala in the treatment of osteoporotic fractures

Objective:To explore the potential mechanism of Astragalus membranaceus and Atractylodes macrocephala in the treatment of osteoporotic fracture (OPF) based on network pharmacology.  Methods:  The active components and action targets of Astragalus membranaceus and Atractylodes macrocephala were screened by pharmacologic database and Analysis Platform (TCMSP) . GeneCards, OMIM and TTD databases related to disease targets were retrieved to screen the action targets of OPF, and then the intersection core targets of Astragalus membranaceus, Atractylodes macrocephala membranaceus and OPF were screened.  Cytoscape 3.7.1 software was used to construct a compound target disease network, and DAVID database was used to analyze the enrichment of GO function and KEGG pathway.  Results: Based on TCMSP database, 19 active components and 115 intersection targets of Astragalus membranaceus Atractylodes for OPF were screened. A total of 568 items were obtained by GO functional enrichment analysis, including 433 biological process items, 43 cell composition items and 92 molecular function items.  KEGG pathway enrichment analysis revealed 111 items, including AGE-RAGE, IL-17, TNF, prostate cancer, Toll-like receptor, HIF-1, NF-κB signaling pathway, etc.  Conclusion: Astragalus membranaceus and Atelectylodes atelectylodes may regulate inflammatory response and internal balance of osteoclasts by regulating TNF, NF-κB and HIF-1 signaling pathways, and thus exert therapeutic actions on OPF.