Effect and Mechanism of Schizandrin A in the Treatment of Liver Cancer Using Network Pharmacology, Molecular Docking, and Target Validation

Background Liver cancer is a common threat to human health. Schizandrin A (SA) has certain therapeutic effect on liver cancer, but its related mechanism of action not clear. Elucidating this great significance for the development drugs target cancer. Objective The objective study and SA Methods potential targets in treatment were screened based network pharmacology, core further by protein interaction. Kyoto Encyclopedia Genes Genomes (KEGG) analysis was performed find key pathways action. results obtained verified vitro pharmacological experiments with HepG2 cells. Specifically, an Enzyme Linked Immunosorbent assay (ELISA) kit used detect content indicators (interleukin-1 (IL-1), Tumor Necrosis Factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-10 (IL-10), superoxide dismutase [SOD], malondialdehyde [MDA], interferon (IFN), Glutathione peroxidase (GSH-px)), Quantitative Real-time Polymerase Chain Reaction (qRT-PCR) messenger Ribonucleic Acid (mRNA) (phosphatidylinositol 3 kinase (PI3K), B (Akt), vascular endothelial growth factor (VEGFA), Transforming Growth Factor Beta-1 (TGF-β1)) after drug intervention, Western blotting (WB) detected expression proteins (p-PI3K, PI3K, p-Akt, Akt). Results showed that mainly acts IL-1β, TNF-α, IL-6, IL-10, SOD, MDA, TGF-β1, IFN, VEGFA, affecting PI3K-Akt signaling pathway playing anti-inflammatory role experimental significantly reduced inflammation level cells; improved oxidative stress state (decreasing SOD increasing MDA cells); downregulated Akt mRNA levels; inhibited pathway. Conclusions significant anti-HepG2 effect, which may be achieved reducing levels, improving state, inhibiting