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  3. Benzo[a]pyrene And Rheumatoid Arthritis: An Integrated Computational Investigation.
  1. Home
  3. Benzo[a]pyrene And Rheumatoid Arthritis: An Integrated Computational Investigation.

Related Experiment Video

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

Benzo[a]pyrene and Rheumatoid Arthritis: An Integrated Computational Investigation.

Yuxin Han1, Guangyao Chen2, Weichao Li1

  • 1Beijing University of Chinese Medicine.

Journal of Visualized Experiments : Jove
|June 15, 2026

View abstract on PubMed

Summary
This summary is machine-generated.

Benzo[a]pyrene (BaP), a pollutant, may trigger rheumatoid arthritis (RA) by interacting with key immune genes. This study reveals BaP

Related Experiment Videos

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

Area of Science:

  • Environmental toxicology
  • Computational biology
  • Rheumatology

Background:

  • Polycyclic aromatic hydrocarbons (PAHs) are environmental pollutants linked to rheumatoid arthritis (RA) pathogenesis.
  • Benzo[a]pyrene (BaP), a prominent PAH, is suspected to contribute to RA onset, but its toxicological mechanisms require elucidation.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying Benzo[a]pyrene's potential role in rheumatoid arthritis development.
  • To identify key genes and pathways affected by BaP exposure in the context of RA.

Main Methods:

  • Integrated network toxicology, machine learning, and molecular docking approaches.
  • Identification and network construction of BaP's RA-related target genes.
  • Gene Ontology (GO) and KEGG pathway enrichment analyses.
  • Topological analysis and machine learning for core gene identification.
  • Molecular docking and dynamics simulations to assess binding affinity.

    • Main Results:

    • Fifteen potential RA-related target genes of BaP were identified, enriched in leukocyte migration and immune signaling pathways (e.g., NF-κB, T cell receptor).
    • Five core genes (LCK, ZAP70, ITK, GZMA, ITGAL) were identified and validated.
    • BaP demonstrated strong binding affinity to the protein products of these core genes, forming stable complexes.

    Conclusions:

    • This study provides a computational framework elucidating BaP's potential mechanisms in RA pathogenesis.
    • Findings offer a theoretical basis for understanding RA development linked to environmental pollutants like BaP.
    • Highlights potential therapeutic targets for RA prevention and treatment.