Objective To explore the mechanism of Wuling Powder（五苓散） in the treatment of diabetic nephropathy（DN） based on network pharmacology. Methods The TCMSP analysis platform

GeneCards database and OMIM database were used to screen the active ingredients

targets and disease targets of the component medicines in Wuling Powder. Take the intersection of drug target and disease target to obtain drug disease target

construct drug component target disease interaction network diagram and protein interaction network diagram（PPI）

infer its core target

and enrich the core target with GO function enrichment analysis and KEGG pathway enrichment analysis. Results A total of 19 effective targets for the treatment of DN were obtained from the screening of Wuling Powder. In the analysis of the protein interaction network

9 key targets with a screening value exceeding the average value were CASP 3

RELA

CASP 8

ESR 1

AR

BCL 2

CASP 9

NR3 C1

and ICAM1. Among them

CASP 3

CASP 8

and CASP 9 are Caspases family proteins

and CASP 3

CASP 8

CASP 9

BCL 2 were apoptosis-related protein. GO function enrichment analysis showed that the effect of Wuling Powder in the treatment of DN was mainly on cell components such as cytoplasm

lipoprotein particles

and organelles; molecular functions involved include lipid binding

cysteine endopeptidase activity and other enzymes molecular binding process. RNA

DNA binding process and enzyme activity were involved in the apoptosis process; it was mainly involved in biological processes such as lipid response

cell apoptosis regulation

and hormone response. Enrichment analysis of the KEGG pathway showed that these targets were involved in cancer

hepatitis B

and diabetes complications

AGE-RAGE signaling pathway by toxoplasmosis

apoptosis

tuberculosis

phosphatidylinositol 3-kinase（PI3 K）/protein kinase B（ Akt） signal pathway and other 142 signal pathways

and the repetition rate of Caspases

BCL2

RELA and other target genes in the pathway was extremely high. Conclusion Wuling Powder may reduce kidney cell damage by regulating apoptosis-related proteins such as Caspases family proteins and BCL2 protein family

thereby delaying the development of DN.