Scholarlink

<p>This study explored the role and molecular mechanisms of dexmedetomidine (DEX), an α2-adrenergic receptor agonist, in the treatment of a mouse model of acute liver injury (ALI). DEX significantly mitigated hepatic tissue damage and reduced serum levels of liver function biomarkers and proinflammatory cytokines. Network pharmacology analysis revealed 81 common targets between DEX and ALI, identifying 10 crucial hub genes. Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated that DEX’s therapeutic effect on ALI is likely linked to the activation of the PI3K/AKT pathway. Immunohistochemical experiments verified DEX’s activation of the PI3K/AKT pathway. Molecular docking and dynamic simulations confirmed the stable interaction between DEX and the epidermal growth factor receptor (EGFR). Immunohistochemistry and western blotting further validated that DEX pretreatment upregulated EGFR expression. Our findings indicate that DEX may mitigate ALI by interacting with EGFR and triggering the PI3K/AKT pathway. These findings provide a solid theoretical and experimental basis for using DEX as a potential therapeutic regimen for treating inflammatory liver diseases.</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

Network pharmacology and experimental validation reveal dexmedetomidine’s protective mechanisms against acute liver injury in mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年3月17日

查看全文
  • Chong Zhang,
  • Yixin Fan,
  • Zhijun Qin,
  • Mi Su,
  • Fu Yao

摘要

This study explored the role and molecular mechanisms of dexmedetomidine (DEX), an α2-adrenergic receptor agonist, in the treatment of a mouse model of acute liver injury (ALI). DEX significantly mitigated hepatic tissue damage and reduced serum levels of liver function biomarkers and proinflammatory cytokines. Network pharmacology analysis revealed 81 common targets between DEX and ALI, identifying 10 crucial hub genes. Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated that DEX’s therapeutic effect on ALI is likely linked to the activation of the PI3K/AKT pathway. Immunohistochemical experiments verified DEX’s activation of the PI3K/AKT pathway. Molecular docking and dynamic simulations confirmed the stable interaction between DEX and the epidermal growth factor receptor (EGFR). Immunohistochemistry and western blotting further validated that DEX pretreatment upregulated EGFR expression. Our findings indicate that DEX may mitigate ALI by interacting with EGFR and triggering the PI3K/AKT pathway. These findings provide a solid theoretical and experimental basis for using DEX as a potential therapeutic regimen for treating inflammatory liver diseases.