Network toxicology and molecular docking techniques to explore the mechanism of bisphenol A on obesity

Area of Science:

• Environmental Health
• Molecular Biology
• Toxicology

Background:

• Bisphenol A (BPA) is a common chemical found in plastics.
• Obesity (OB) is a complex metabolic disease with significant public health implications.
• Understanding the molecular links between environmental toxins like BPA and obesity is crucial for prevention.

Purpose of the Study:

• To investigate the molecular mechanisms by which Bisphenol A (BPA) exposure may contribute to obesity (OB).
• To identify key molecular targets and signaling pathways involved in BPA-induced obesity.
• To propose a novel research approach for assessing the health impacts of chemical toxins.

Main Methods:

• Utilized multiple databases (CTD, STITCH, DrugBank, GeneCards, OMIM) to identify 237 potential targets for BPA and OB.
• Employed network analysis tools (STRING, Cytoscape) to pinpoint 10 key molecular targets.
• Performed enrichment analysis (DAVID) to determine associated signaling pathways.
• Conducted molecular docking and dynamics simulations to assess BPA binding affinity to target proteins.

Main Results:

• Identified 10 key molecular targets, including INS, IL-6, AKT1, and PPARG, associated with BPA exposure and OB.
• Enrichment analysis revealed involvement in PI3K-Akt and Insulin signaling pathways.
• BPA demonstrated strong molecular binding to INS, IL-6, AKT1, and PPARG, with stable complex formation observed for BPA and PPARG.
• BPA influences apoptosis, proliferation, inflammatory signaling, and insulin resistance, linking it to OB development.

Conclusions:

• BPA exposure may promote obesity by disrupting key cellular processes and signaling pathways.
• The identified molecular targets and pathways provide insights into BPA's role in obesity pathogenesis.
• Findings support preventative strategies against obesity linked to BPA exposure from plastic products and contaminated environments.