The Mechanism of Cordymin for Treating Osteoporosis: Integrated Network Pharmacology, Bioinformatics Analyses, and Animal Experiments.

Osteoporosis (OP), a systemic skeletal disorder characterized by low bone mass and microarchitectural deterioration of bone tissue, leads to increased bone fragility and fracture susceptibility. This study investigated the therapeutic potential of cordymin against OP through integrated network pharmacology and animal experiments. Cordymin and OP-related targets were retrieved from public databases. Protein-protein interaction (PPI) network of potential targets was constructed using STRING database and visualized using Cytoscape software. The potential targets Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were enriched via the bioinformatics website. Molecular docking was performed using Autodock Vina software and animal experiments were conducted to verify the mechanism of cordymin treatment of OP. Network pharmacology analysis revealed sixty intersection targets between cordymin and OP and identified eight core targets. The main enrichment pathways included Forkhead box O (FoxO) signaling pathway, PI3K-Akt signaling pathway and lipid and atherosclerosis. Molecular docking results showed that cordymin demonstrated stable binding to the eight core targets. Animal experiments showed that cordymin treatment significantly upregulated the expression of CCND1 and ALB in the femur compared with the model group. This study predicted the core target and pathway of cordymin in against OP treatment by network pharmacology, and verified these findings through animal experiments, which provided a basis for further study of its pharmacological mechanism.