Scholarlink

<p>The increasing prevalence of mycotoxin toxicity poses significant health risks, contributing to various diseases. Among these, fumonisin B1 (FB<sub>1</sub>) alters sphingolipid biosynthesis, induces oxidative stress, apoptosis, mitochondrial dysfunction, and inflammation. This study investigated the impact of acute FB<sub>1</sub> exposure on inflammation and epigenetics changes in hearts of C57BL/6 mice. Molecular docking was performed to identify potential interactions between FB<sub>1</sub> and key inflammatory proteins (TNF-α, iNOS, NF-κB p65, and NF-κB p50). Excised C57BL/6 mice heart tissue was analysed for gene expression (qPCR), protein expression (Western blotting), nitric oxide levels (NOS assay), cytokine levels (ELISA), and global DNA methylation (ELISA). Molecular docking suggested FB<sub>1</sub> interacted with key residues in TNF-α, iNOS, and NF-κB, potentially influencing their activity. Gene expression analysis (<i>TNF-α, NF-κB</i><i>, </i><i>IL-6, NLRP3 Inflammasome, IL-18, caspase 1, IL-1β, GSDMD, caspase 3, CT-1, IL-10, MBD2, DNMT1, DNMT3A, and DNMT3B</i>) revealed that FB<sub>1</sub> significantly dysregulated inflammatory cytokines and DNA methylation-related genes. Protein expression analysis showed significant upregulation of pro-inflammatory cytokines (TNF-α, NF-κB, IL-6, IL-1β, IL-18, IL-10, and TGF-β1). Global DNA methylation levels were significantly increased, with notable upregulation of DNMT1. In conclusion, acute exposure of C57BL/6 mice to FB<sub>1</sub> significantly impacted inflammatory and DNA methylation pathways, leading to cardiac distress complications.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Fumonisin B1 exposure induces cardiac inflammation in C57BL/6 mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月31日

查看全文
  • Selwyn Gounder,
  • Ndumiso Mhlongo,
  • Terisha Ghazi,
  • Anil Chuturgoon

摘要

The increasing prevalence of mycotoxin toxicity poses significant health risks, contributing to various diseases. Among these, fumonisin B1 (FB1) alters sphingolipid biosynthesis, induces oxidative stress, apoptosis, mitochondrial dysfunction, and inflammation. This study investigated the impact of acute FB1 exposure on inflammation and epigenetics changes in hearts of C57BL/6 mice. Molecular docking was performed to identify potential interactions between FB1 and key inflammatory proteins (TNF-α, iNOS, NF-κB p65, and NF-κB p50). Excised C57BL/6 mice heart tissue was analysed for gene expression (qPCR), protein expression (Western blotting), nitric oxide levels (NOS assay), cytokine levels (ELISA), and global DNA methylation (ELISA). Molecular docking suggested FB1 interacted with key residues in TNF-α, iNOS, and NF-κB, potentially influencing their activity. Gene expression analysis (TNF-α, NF-κB, IL-6, NLRP3 Inflammasome, IL-18, caspase 1, IL-1β, GSDMD, caspase 3, CT-1, IL-10, MBD2, DNMT1, DNMT3A, and DNMT3B) revealed that FB1 significantly dysregulated inflammatory cytokines and DNA methylation-related genes. Protein expression analysis showed significant upregulation of pro-inflammatory cytokines (TNF-α, NF-κB, IL-6, IL-1β, IL-18, IL-10, and TGF-β1). Global DNA methylation levels were significantly increased, with notable upregulation of DNMT1. In conclusion, acute exposure of C57BL/6 mice to FB1 significantly impacted inflammatory and DNA methylation pathways, leading to cardiac distress complications.