# Potential mechanisms and effects of AFB1-induced asthma: A comprehensive analysis based on network toxicology and molecular docking

## TL;DR

This study explores how aflatoxin B1 may cause asthma by identifying key molecular targets and signaling pathways involved in the process.

## Contribution

The study provides new insights into the molecular mechanisms of aflatoxin B1-induced asthma using network toxicology and molecular docking.

## Key findings

- AFB1 exposure is linked to asthma through targets like PTGS2, ADRB2, and CysLTR1.
- Neuroactive ligand-receptor interactions and calcium signaling pathways are central to AFB1-induced asthma.
- Molecular docking confirmed strong affinity between AFB1 and key asthma-related targets.

## Abstract

The aim of this study was to systematically explore the potential molecular mechanisms by which aflatoxin B1 (AFB1) may trigger asthma using network toxicology and molecular docking. Potential targets related to asthma caused by AFB1 were obtained from databases, such as PubChem, ProTox, ADMETab, and GeneCards. The targets most significantly related to asthma were further screened using STRING and Cytoscape and analyzed using GO and KEGG enrichment. Finally, molecular docking and visualization were performed using AutodockVina 1.2.2 and PyMOL 2.5 to further determine the affinity between AFB1 and the core targets. We identified 31 potential targets associated with AFB1 exposure and asthma, including PTGS2, ADRB2, CysLTR1, PTGS1, and others. The enrichment analysis revealed that the core targets of AFB1-induced asthma were neuroactive ligand‒receptor interactions, the calcium signaling pathway, and the adipocyte catabolism-related signaling pathway. Molecular docking results revealed that AFB1 exhibited good affinity for the core targets. In the present study, the potential mechanisms involved in AFB1-induced asthma were elucidated, new insights into how environmental toxins trigger asthma were provided, and a theoretical foundation for asthma prevention and treatment was established.