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一项综合性脂组学和转录学研究显示,巴瓦辛和伊卡林协同诱导特异性肝损伤
Yingying Li1,2, Bo Cao1, Mengmeng Lin1
1National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Immunopharmacology and immunotoxicology
|November 6, 2024
概括
传统中医药 (TCM) 的成分巴瓦和伊卡林,当与TNF-α相结合时,可以导致肝损伤. 这项研究揭示了改变的脂质代谢和基因表达途径,有助于在特异性药物诱导性肝损伤 (IDILI) 中产生这种协同效应.
科学领域:
- 药理学和毒理学 药理学和毒理学
- 肝病学 肝病学是一种肝病学.
- 传统中医研究 传统中医研究
背景情况:
- 越来越多的与传统中医 (TCM) 相关的肝损伤报告强调了识别致病原体和机制的挑战.
- Psoraleae Fructus (PF) 和Epimedii Folium (EF) 是常见的TCM成分,涉及特异性药物诱导性肝损伤 (IDILI),但它们的具体作用尚不清楚.
研究的目的:
- 为了确定 PF 和 EF 中的易感性成分,这些成分有助于 IDILI.
- 利用脂管学和转录学阐明这些TCM组件诱导的IDILI的潜在机制.
主要方法:
- 利用TNF-α介导的小鼠模型来研究肝损伤.
- 确定了巴巴 (Bav) 和伊卡林 (Ica) 作为关键成分.
- 采用脂组学和转录学来分析代谢和基因表达变化.
主要成果:
- 同时暴露于Bav,Ica和TNF-α导致严重的肝损伤,与单个暴露不同.
- 脂类体检显示了阿尔法-烯酸,阿拉基酸和酸代谢的改变.
- 转录组学发现了与PI3K/AKT/mTOR信号传递和脂代谢相关的差异性基因表达.
结论:
- 巴瓦和伊卡林与TNF-α协同作用,诱导IDILI.
- 细胞内代谢和基因表达的改变是关键机制.
- 研究结果提供了关于TCM诱导的肝损伤和潜在生物标志物的见解.
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