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Background <p>Bisphenol A (BPA), a widespread environmental endocrine disruptor, has raised concerns for its neurotoxic effects, yet its molecular role in stroke remains unclear.</p> Methods <p>BPA target genes were retrieved from ChEMBL, DrugBank, and SwissTargetPrediction. Differentially expressed genes (DEGs) and key co-expression modules related to stroke were identified from the GSE16561 dataset using weighted gene co-expression network analysis (WGCNA). Core targets were determined by overlapping BPA targets, DEGs, and genes within significant WGCNA modules, followed by protein–protein interaction (PPI) network analysis. Functional enrichment was conducted using DAVID, and molecular docking assessed BPA’s binding affinity to the identified core targets.</p> Results <p>Analysis of GSE16561 identified 1,801 DEGs. Intersection with BPA targets and WGCNA module genes yielded 22 candidate genes. PPI network topology analysis (MCC, closeness, degree) highlighted 10 core targets: NDUFB7, NDUFA11, NDUFB11, NDUFB8, NDUFS8, NDUFA12, NDUFS5, NDUFA8, NDUFV1, and NDUFA13. Functional enrichment revealed 12 significant Gene Ontology terms and 14 KEGG pathways. Molecular docking demonstrated stable binding of BPA to all 10 core targets, with NDUFA11 (− 7.7&#xa0;kcal/mol) and NDUFV1 (− 7.4&#xa0;kcal/mol) exhibiting the highest binding affinities.</p> Conclusion <p>This study is the first to systematically elucidate the role of BPA exposure in stroke and its potential molecular mechanisms, providing important evidence for understanding the toxicological effects of BPA. In addition, it offers a theoretical basis for developing strategies to prevent and mitigate cerebrovascular injury associated with BPA exposure.</p> Clinical trial number <p>Not applicable.</p>

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Integrative network toxicology, transcriptomic, and molecular docking approaches to elucidate the toxicity and mechanisms of bisphenol A in stroke

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月27日

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  • Zhonghui Wen,
  • Bin Hu,
  • Qiongfang Zhang,
  • Zhifu Sun,
  • Hai Wang,
  • Kun Zhang,
  • Jingchun Pei,
  • Ziyu Chen

摘要

Background

Bisphenol A (BPA), a widespread environmental endocrine disruptor, has raised concerns for its neurotoxic effects, yet its molecular role in stroke remains unclear.

Methods

BPA target genes were retrieved from ChEMBL, DrugBank, and SwissTargetPrediction. Differentially expressed genes (DEGs) and key co-expression modules related to stroke were identified from the GSE16561 dataset using weighted gene co-expression network analysis (WGCNA). Core targets were determined by overlapping BPA targets, DEGs, and genes within significant WGCNA modules, followed by protein–protein interaction (PPI) network analysis. Functional enrichment was conducted using DAVID, and molecular docking assessed BPA’s binding affinity to the identified core targets.

Results

Analysis of GSE16561 identified 1,801 DEGs. Intersection with BPA targets and WGCNA module genes yielded 22 candidate genes. PPI network topology analysis (MCC, closeness, degree) highlighted 10 core targets: NDUFB7, NDUFA11, NDUFB11, NDUFB8, NDUFS8, NDUFA12, NDUFS5, NDUFA8, NDUFV1, and NDUFA13. Functional enrichment revealed 12 significant Gene Ontology terms and 14 KEGG pathways. Molecular docking demonstrated stable binding of BPA to all 10 core targets, with NDUFA11 (− 7.7 kcal/mol) and NDUFV1 (− 7.4 kcal/mol) exhibiting the highest binding affinities.

Conclusion

This study is the first to systematically elucidate the role of BPA exposure in stroke and its potential molecular mechanisms, providing important evidence for understanding the toxicological effects of BPA. In addition, it offers a theoretical basis for developing strategies to prevent and mitigate cerebrovascular injury associated with BPA exposure.

Clinical trial number

Not applicable.