Integrating network toxicology and molecular docking to explore the toxicity of the environmental pollutant butyl hydroxyanisole: An example of induction of chronic urticaria

The study aimed to comprehensively investigate environmental pollutants’ potential toxicity and underlying molecular mechanisms, focusing on chronic urticaria (CU) induced by butylated hydroxyanisole (BHA) exposure, further drawing public awareness regarding the potential risks of environmental pollutants, applying ChEMBL, STITCH, and SwissTargetPrediction databases to predict the targets of BHA, CTD, GeneCards, and OMIM databases to collect the relevant targets of CU. Ultimately, we identified 81 potential targets of BHA-induced CU and extracted 31 core targets, including TNF, SRC, CASP3, BCL2, IL2, and MMP9. GO and KEGG enrichment analyses revealed that these core targets were predominantly involved in cancer signaling, estrogen and endocrine resistance pathways. Furthermore, molecular docking confirmed the ability of BHA to bind with core targets. The onset and development of CU may result from BHA by affecting multiple immune signaling pathways. Our study elucidated the molecular mechanisms of BHA toxicity and its role in CU induction, providing the basis for preventing and treating chronic urticaria associated with environmental BHA exposure. [Display omitted] •Integrating network toxicology and molecular docking to explore the toxicity of butyl hydroxyanisole, may induce chronic urticaria by modulating core targets such as TNF, SRC, CASP3, BCL2, IL2, and MMP9.•Furthermore, butyl hydroxyanisole may induce the onset of chronic urticaria through multi-pathways such as PI3K-AKT signaling pathway and cancer-related pathways.•This study promotes the application of network toxicology and molecular docking techniques in the study of toxicity and mechanisms of other environmental pollutants.