Investigating the Aidi injection mechanism for low-grade glioma based on the network pharmacology approach, The Cancer Genome Atlas (TCGA), and molecular docking technology.

Low-grade glioma (LGG) can affect any part of the central nervous system. This study aimed to investigate the mechanism of Aidi injection (AIDI) in treating LGG using network pharmacology, The Cancer Genome Atlas, and molecular docking technology. Open databases were used to obtain AIDI targets and components as well as LGG genes. To identify essential elements and targets, a protein-protein interaction network and an active ingredient-common target network were built. Kyoto encyclopedia of genes and genomes and gene ontology enrichment analysis were used to screen the major signaling pathways. The clinical importance of key genes was confirmed using both survival and differential expression studies. The top 6 components in terms of degree value on the active ingredient-common target network were considered as the core components of AIDI for treating LGG. CASP3, TGFβ1, TP53, and EGFR were termed hub target genes, which are not only aberrantly expressed in LGG tissue, but their excessive expression was also found to lower patient survival rates. The biological processes linked to the antitumor activity of AIDI primarily involve responses to hormones and reactive oxygen species. Kyoto encyclopedia of genes and genomes enrichment analysis identified PI3K-AKT and MAPK as the most important signaling pathways. Molecular docking experiments demonstrated strong binding between the hub genes and the essential components of AIDI. AIDI may target CASP3, TGFβ1, TP53, and EGFR and modulates PI3K-AKT and MAPK signaling pathways to exert its anticancer action against LGG. Reactive oxygen species may play an important role in this process.