网络毒理学和分子对接分析抗结核病药物诱导肝毒性
Rui Liu1, Xinlei Liu2,3, Yancheng Wang4
1Institute for Immunology and Pathogenesis, Chongqing Medical University, Chongqing, China.
Journal of biochemical and molecular toxicology
|November 11, 2025
概括
抗结核药物诱导的肝毒性 (DIH) 可以伤害患者. 这项研究确定了关键的分子标和途径,揭示了氧化应激和亡作为机制,为肝脏保护策略提供了见解.
科学领域:
- 毒理学 毒理学 毒理学
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 药物诱导的肝毒性 (DIH) 是抗结核病 (抗结核病) 治疗的显著不良影响.
- DIH经常导致治疗中断和患者不良后果.
研究的目的:
- 阐明抗结核药物引起的肝毒性背后的分子机制.
- 确定涉及DIH的关键分子标和信号通路.
主要方法:
- 综合网络毒理学,分子对接和体内实验.
- 分析了药物 - 疾病交叉点 - 目标相互作用和途径丰富.
- 评估了抗结核药物与点点的结合亲和力,并在体内验证了mRNA表达.
主要成果:
- 确定了NFE2L2,NFKB1,MAP2K1,MAPK14,IGF1R和GSK3B作为DIH的潜在关键目标.
- 突出了氧化应激,亡和脂质积累作为潜在的机制.
- 通过体内实验验验证了核心目标mRNA表达的变化.
结论:
- 提供了对抗结核病药物诱导的肝毒性分子基础的更深入的理解.
- 建议在结核病治疗期间开发肝脏保护策略的潜在分子标.
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