Analysis on Mechanism of Astragali Radix in Treating IgA Nephropathy Based on Network Pharmacology and in Vitro Cell Experiment
10.13422/j.cnki.syfjx.20210848
- VernacularTitle:基于网络药理学和体外细胞实验分析黄芪治疗IgA肾病的作用机制
- Author:
Shuang PANG
1
;
Shuan ZHAO
2
;
Xia-lian XU
2
;
Jia-wei YU
2
;
Xiao-qiang DING
1
Author Information
1. Fudan University，Shanghai 200433，China
2. Shanghai Key Laboratory of Kidney Disease and Blood Purification，Shanghai Clinical Medical Center of Kidney Disease，Zhongshan Hospital Affiliated to Fudan University，Shanghai 200032，China
- Publication Type:Research Article
- Keywords:
Astragali Radix;
immunoglobulin A （IgA）;
IgA nephropathy;
network pharmacology;
astragaloside Ⅳ;
molecular mechanism;
in vitro cell test
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2021;27(15):139-147
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the multi-component， multi-target and multi-pathway mechanism of Astragali Radix against immunoglobulin A nephropathy （IgAN） by network pharmacology， aiming to provide evidence for its basic research and clinical application. Method:The active chemical components and targets of Astragali Radix and targets associated with IgAN were obtained by literature mining and GeneCards， Traditinal Chinese Medicine Integrated Database （TCMID）， Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP） databases. Cytoscape 3.7.1 software was used to draw network interaction diagrams. The key targets of Astragali Radix against IgAN were searched by network topology. Gene ontology （GO） analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway analysis involved in the targets were analyzed by different packages in R programming language. On this basis， cell experiments in vitro were carried out to verify the activation effect of astragaloside Ⅳ on phosphatidylinositol 3-kinase/protein kinase B/tumor suppressor gene protein 53 （PI3K/Akt/p53） signaling pathway of human mesangial cells. Result:A total of 25 active components and 49 ingredient-disease targets of Astragali Radix were screened. The GO enrichment analysis included 84 items， which were related to nuclear hormone receptor binding， nuclear receptor activity， deoxyribonucleic acid binding transcriptional activation activity and other aspects. The KEGG pathway enrichment analysis included 88 KEGG pathways， which were closely related to PI3K/Akt signaling pathway， hypoxia inducible factor-1 （HIF-1） signaling pathway， advanced glycation end product/receptor of advanced glycation end product （AGE/RAGE） signaling pathway and others. Cell experiments in vitro confirmed that astragaloside Ⅳ could effectively inhibit the platelet derived growth factor-BB （PDGF-BB）-induced proliferation of human mesangial cells by regulating PI3K/Akt/p53 signaling pathway. Conclusion:The active ingredients of Astragali Radix may play a role in the treatment of IgAN by acting on targets and pathways related to apoptosis， oxidative stress， inflammation response and others， providing ideas and directions for the new drug development and mechanism study of IgAN.
