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代谢分析显示ADB-BUTINACA诱导的长期肝毒性

Siyue Zheng¹, Yi Zhou², Xiaoran Song³

¹College of Chemical Engineering, Zhejiang University of Technology, Hangzhou, 310014, China.

Chemico-biological interactions

|September 25, 2025

概括

合成大麻素ADB-BUTINACA会导致肝脏损伤并破坏脂质代谢. 这项研究揭示了它对脂肪酸和TCA循环途径的毒性影响,突出了与这种新兴污染物相关的风险.

科学领域:

毒理学毒理学毒理学
代谢学代谢学代谢学
药理学药理学是一个学科.

背景情况:

ADB-BUTINACA是一种合成大麻素,具有很高的滥用潜力和已知的多器官毒性.
目前尚不清楚ADB-BUTINACA的长期毒理作用和代谢机制.
了解这些影响对于公共卫生风险评估至关重要.

研究的目的:

为了研究ADB-BUTINACA.的肝毒性潜力.
为了阐明ADB-BUTINACA引起的代谢干扰.
探索ADB-BUTINACA诱导的肝损伤背后的分子机制.

主要方法:

在小鼠中使用ADB-BUTINACA在不同剂量 (0.1,1,10毫克/公斤) 的30天口服暴露模型.
血清生物化学分析,组织病理学,非向代谢学,RT-qPCR和分子对接.
分析关键的代谢途径和酶相互作用.

主要成果:

ADB-BUTINACA诱导的剂量依赖性肝损伤,全身炎症和脂质失调 (TNF-α,IL-6,胆固醇,甘油三,LDL-C的升高).
代谢分析确定了60种改变的代谢物和12种扰乱的途径,包括不和脂肪酸生物合成和TCA循环.
观察到EPA,DHA和牛的水平降低,有证据表明ADB-BUTINACA抑制TCA循环和脂肪酸合成酶 (FADS2,ELOVL2).

结论:

ADB-BUTINACA通过代谢中断引起显著的肝毒性,特别是影响脂质代谢和TCA循环.
该化合物通过结合FADS2和ELOVL2.2等关键酶来干扰内源性脂质调节.
这些发现凸显了ADB-BUTINACA作为新兴合成大麻素污染物的潜在健康风险.

关键词:

在ADB-BUTINACAA中使用.肝毒性肝毒性肝毒性炎症炎症是一种炎症.分子对接是分子对接.非向的代谢基因组.

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