在HT22细胞中通过介导PERK信号通路和ROS相互作用来诱导Dibromoacetonitrile自
Fang Li1, Xueyu Zhu2, Xinwei Xu1
1School of Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, China.
Toxicology
|December 8, 2023
概括
饮用水污染物的二甲 (DBAN) 通过激活内分泌网膜应激 (ERS) 和自途径引起神经毒性. 针对这些通路可能有助于预防DBAN诱导的细胞损伤.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 环境健康 环境健康
背景情况:
- 双酸 (DBAN) 是一种在饮用水中发现的危险的酸 (HAN).
- 暴露于DBAN与神经毒性有关,涉及反应性氧物种 (ROS).
- 在HAN诱导的亡中,细胞内网膜应激 (ERS) 和自的作用尚未完全理解.
研究的目的:
- 调查ERS和自在HT22细胞中DBAN诱导的神经毒性的参与.
- 阐明ROS,ERS和自在DBAN细胞效应中的关系.
- 确定减轻DBAN神经毒性的潜在治疗点.
主要方法:
- 用DBAN (10微米,24小时) 治疗HT22细胞.
- 通过使用4-phenylbutyric acid (4-PBA) 来抑制ESR.
- 使用3-甲基氨酸 (3-MA) 抑制了自.
- 抗氧化剂N-乙半氨酸 (NAC) 用于评估ROS的参与.
主要成果:
- DBAN激活了ERS PERK信号通路,导致细胞毒性.
- DBAN诱导了自,从而调解了细胞毒性.
- ERS抑制 (4-PBA) 降低了DBAN诱导的亡和自.
- 抗氧化剂 (NAC) 和ERS抑制 (4-PBA) 降低了ROS的产生.
- 发现ROS和ERS形成了积极的反循环,促进了自和细胞损伤.
结论:
- 在HT22细胞中,DBAN通过ERS和自诱导神经毒性.
- PERK信号通路和ROS相互作用调解了DBAN诱导的自.
- ERS-PERK信号传递促进了DBAN诱导的自.
- 准ERS,自和ROS可能是预防HAN诱导的神经毒性的策略.
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