Exploring the mechanism of PPCPs on human digestive system-related chronic inflammatory diseases based on network toxicology and molecular docking.

Pharmaceutical and personal care products (PPCPs), emerging pollutants, may cause chronic inflammatory and metabolic diseases by inducing metabolic disorders. To explore the underlying mechanisms, this study used network toxicology and molecular docking, focusing on four representative diseases: digestive system diseases, rheumatoid arthritis (RA), non-alcoholic fatty liver disease (NAFLD), and Parkinson's disease. By integrating data from GeneCards, OMIM, and STRING databases, we found 255, 132, 128, and 117 intersection targets between PPCPs and these diseases respectively. Protein-protein interaction (PPI) networks highlighted core hubs like BCL2, IL1B, and PTGS2. Molecular docking showed strong binding affinities (e.g., IL1ß: -22.18 kcal/mol; CASP3: -23.23 kcal/mol). GO/KEGG analyses revealed PPCPs disrupt shared pathways, such as the AGE - RAGE signaling in digestive diseases and RA, PI3K-Akt-mediated insulin resistance in NAFLD, and neuroinflammation via PTGS2 inhibition in Parkinson's. Notably, 90 % of top hub genes (e.g., STAT3, AKT1) overlapped across diseases, forming an "inflammation-apoptosis" axis. Our findings suggest PPCPs may exert toxicity through cross-organ interactions via conserved molecular networks, offering insights for environmental risk assessment and cross-disease therapeutic strategy development.