暴露于会通过NFκB p65/RBBP4/Survivin信号通路诱导神经元亡
Hui Chen1, Wei Zhang1, Song Luo2
1Department of Anatomy, School of Medicine, Nanchang University, BaYi Road 461, Nanchang 330006, PR China.
Toxicology
|October 22, 2023
概括
暴露促进神经元亡,通过通过NFκB p65通路降低RBBP4和Survivin的调节. 恢复RBBP4水平可以减轻诱导的细胞死亡,提供治疗见解.
科学领域:
- 神经科学是一个神经科学.
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- (Pb) 是一种无处不在的重金属毒素,影响多个器官系统.
- 细胞亡,或编程细胞死亡,对于神经系统的发展和稳定性至关重要.
- RB结合蛋白4 (RBBP4) 与神经元亡有关,但其在暴露中的作用尚不清楚.
研究的目的:
- 调查RBBP4在因暴露引起的神经元亡中的作用.
- 为了阐明参与诱导的神经元细胞死亡的信号通路.
主要方法:
- PC12细胞和老鼠海马被暴露于酸 (PbAc).
- 用TUNEL测试来评估细胞亡.
- 对RBBP4,Survivin和NFκB p65的mRNA和蛋白质水平进行了分析.
- 进行了NFκB p65抑制和RBBP4过度表达.
主要成果:
- 暴露显著增加了PC12细胞和老鼠海马细胞的亡.
- 暴露降低了RBBP4和Survivin的表达,同时增加了NFκB p65.
- 抑制NFκB p65逆转了RBBP4.4的减少.
- 过度表达RBBP4可减少诱导的亡并增加生存率.
结论:
- 暴露于会通过NFκB p65/RBBP4/Survivin信号通路诱导神经元亡.
- RBBP4作为一种保护因子,对诱导的神经细胞亡起作用.
- 针对这种途径可能提供减轻毒性的策略.
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