Study on the Mechanism for Danggui Anti-carbon Ion Radiation Based on Network Pharmacology

To study the possible mechanism of Danggui anti-carbon ion radiation based on network pharmacology. The Danggui active ingredients and the targets were obtained from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and literature mining. Carbon ion radiation targets were obtained from GeneCard database. The intersection targets of the active ingredient targets and the carbon ion radiation targets were the potential targets for Danggui anti-carbon ion radiation. Active ingredients - potential targets network was constructed. Functional enrichment and pathway enrichment analysis of potential targets were performed. The protein-protein interaction (PPI) network of the potential targets was constructed and the the hub targets were obtained. Molecular docking between the hub targets and active ingredients was performed to verify the results of network pharmacology. A total of nine Danggui active ingredients and ninety-eight potential targets of Danggui anti-carbon ion radiation were obtained. The main active ingredients of Danggui anti-carbon ion radiation were ferulic acid, ligustilide, sitosterol and stigmasterol. Functional enrichment analysis showed that potential targets were primarily engaged in biological processes such as cellular stress response, inflammatory response, kinase activity, as well as molecular functions such as DNA binding, kinase binding, and nuclear receptor activity. Pathway enrichment analysis showed potential targets were mainly involved in PI3K-Akt signaling pathway, MAPK signaling pathway, etc, which interact with each other. PPI network showed that VEGFA, EGFR, CTNNB1, etc. were the hub targets of Danggui anti-carbon ion radiation. The molecular docking results showed that the active ingredient has a good binding activity to the hub targets.This study indicated that Danggui anti-carbon ion radiation was mainly through regulating inflammatory reaction, immune response, cell apoptosis and survival, and damage repair.