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由于暴露于迪奥斯布尔B,导致乙-CoA乙转移酶2的干扰

Yunfang Jiang^1,2,3, Rong Tan⁴, Hui Yang^1,5,6

¹State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Engineering Research Center for the Development and Application of Ethnic Medicine and TCM (Ministry of Education), Guizhou Provincial Engineering Research Center for the Development and Application of Ethnic Medicine and TCM, Guizhou Medical University, Guiyang 550004, P. R. China.

Chemical research in toxicology

|April 11, 2025

概括

来自传统中医药的迪奥斯布林B 迪奥斯科雷亚bulbifera L. 修饰蛋白质,抑制乙-CoA乙转移酶2 (ACAA2) 和破坏脂质代谢.

科学领域:

生物化学生物化学
毒理学毒理学毒理学
药理学药理学是指药理学的学科.

背景情况:

黄 (Dioscorea bulbifera L.) (DBL) 是一种传统的中医药.
它的主要毒性成分是迪奥斯布尔B (DSB).
代谢激活DSB产生cis-enedial (DDE),它与蛋白质残留物发生反应.

研究的目的:

为了研究DSB毒性的机制.
为了识别由DSB衍生的DDE修饰的蛋白质.
为了阐明蛋白质修饰的功能后果.

主要方法:

基于活动的协同质量标记蛋白质概况 (TMT-ABPP).
免疫沉和LC-MS/MS. 这两种方式.
分子对接分析. 分子对接分析.
在体外和体内生物抑制测定.

主要成果:

由DSB衍生的DDE修改了蛋白质中的氨酸 (Cys) 和氨酸 (Lys) 残留物.
肝乙-CoA乙转移酶2 (ACAA2) 被确定为一种标蛋白,在Cys128和Lys143.3中进行修改.
通过DSB/DDE抑制ACAA2的发生方式依赖于度和剂量.
在体内,DSB治疗导致甘油三积累,降低了乙辅酶A水平.

结论:

DSB诱导的毒性涉及到ACAA2.2的修饰和抑制.
ACAA2的添加破坏了脂质代谢,导致三糖的积累.
这项研究揭示了DBL/DSB毒性的分子机制.

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