乌头通过启动ROS线粒体凋亡和Nox5/DJ-1信号通路引发神经毒性和帕金森样症状

BMEMat Pub Date : 2023-06-27 DOI:10.1002/bmm2.12033
Meijun Pang, Xin Song, Yaodong Miao, Yiwen Wang, Chang Zhou, Zihan Geng, Jiayin Du, Bernard Moussian, Yanfang Su, Xiuyun Liu, Dong Ming
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引用次数: 0

摘要

本文编号10.1002/bmm2.12033,庞美君、宋昕及其同事系统地研究了川乌对斑马鱼幼虫神经毒性的分子机制。他们首先评估了整个大脑的神经元活动,发现端脑对川乌毒性最敏感。此外,他们发现川乌上调了nox5基因,下调了dj1基因,导致ROS产生过多和线粒体介导的细胞凋亡,从而导致斑马鱼幼虫的神经毒性作用和帕金森样行为。这对乌头属植物的毒性预防和解毒具有广泛的理论意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Aconitum carmichaelii triggers neurotoxicity and Parkinson-like symptoms through initiation of ROS-mitochondrial apoptosis and the Nox5/DJ-1 signaling pathway

Aconitum carmichaelii triggers neurotoxicity and Parkinson-like symptoms through initiation of ROS-mitochondrial apoptosis and the Nox5/DJ-1 signaling pathway

In this article number 10.1002/bmm2.12033, Meijun Pang, Xin Song and their co-workers systematically studied the molecular mechanism of neurotoxicity of zebrafish larvae caused by Aconitum carmichaelii (Chuanwu). They first assessed neuronal activity in the whole brain and found that the telencephalon was most sensitive to Chuanwu toxicity. Additionally, they found t-hat Chuanwu upregulated the nox5 gene and downregulated the dj1 gene, leading to excessive ROS production and mitochondrial mediated cell apoptosis, which resulted in neurotoxic effects and Parkinson-like behaviors in zebrafish larvae. This has extensive theoretical significance in the field of toxicity prevention and detoxification of Aconitum.

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