Computational Elucidation of the Antidiabetic Mechanism of Catechin and Apigenin via Network Pharmacology and Molecular Docking

Abstract

Insulin resistance, poor glucose homeostasis, oxidative stress, inflammation, and pancreatic β-cell dysfunction are the hallmarks of Type 2 Diabetes Mellitus (T2DM), a chronic metabolic disease. The search for safer multitarget therapeutic agents made from natural products is necessary due to the rising incidence of type 2 diabetes and the drawbacks of traditional antidiabetic treatments. Apigenin and catechin have anti-inflammatory, antihyperglycemic, insulin-sensitizing, and antioxidant qualities. The current study examined the therapeutic mechanisms of apigenin and catechin against type 2 diabetes using integrated network pharmacology and molecular docking techniques. Protein-protein interaction (PPI), Gene Ontology (GO), and KEGG pathway enrichment studies were performed after T2DM-associated genes and potential phytochemical targets were found using publically accessible databases. Important hub genes linked to insulin signaling and glucose metabolism were found by network analysis, including PIK3R1, ESR1, AKT1, EGFR, and PTK2. PI3K-Akt and endocrine resistance pathways were significantly enriched, according to KEGG analysis. Catechin has a strong binding affinity for PIK3R1 (-6.1 kcal/mol) and AKT1 (-6.4 kcal/mol) according to molecular docking, whereas Apigenin had docking scores of -5.7 and -6.3 kcal/mol, respectively, when compared to Metformin. These results offer a scientific foundation for additional experimental confirmation and imply that catechin and apigenin may have antidiabetic effects through multitarget regulation.