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在创伤性脑损伤中识别和验证内质网膜压力相关基因

Gengshui Zhao¹, Yongqi Fu², Chao Yang³

¹Department of Neurosurgery, The People's Hospital of Hengshui City, Hengshui, 053000, Hebei, China. zhaogengshui@163.com.

Journal of molecular neuroscience : MN

|September 12, 2024

概括

在创伤性脑损伤 (TBI) 中,内质网膜应激 (ERS) 是至关重要的. NFE2L2基因激活保护神经元免受ERS诱导的亡,为TBI提供了潜在的治疗标.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

细胞内膜网膜应激 (ERS) 与创伤性脑损伤 (TBI) 的病理生理学有关.
确定与ERS相关的TBI中的关键分子参与者对于治疗开发至关重要.

研究的目的:

用生物信息学和体外实验来识别和验证与TBI相关的ERS相关基因.
研究NFE2L2基因及其编码蛋白Nrf2在缓解TBI中ERS诱导的亡中的作用.

主要方法:

来自GeneCards和CTD数据库的19个TBI和ERS相关基因的生物信息分析.
使用cytoHubba进行蛋白质与蛋白质相互作用 (PPI) 网络分析,以确定枢纽基因,特别是NFE2L2.
在体外细胞实验中,使用三乙基 (tBHQ) 诱导Nrf2,并评估其对ERS和亡的影响,在初级神经元损伤模型中.

主要成果:

对已识别的基因的丰富分析表明,与亡途径的首要联系.
NFE2L2被确定为PPI网络中的中心枢纽基因.
在受到损伤的初级培养神经元中,tBHQ预处理显著降低了ERS和与亡相关的蛋白质表达.

结论:

在创伤性脑损伤的背景下,NFE2L2/Nrf2通路对内质网膜压力诱导的亡起着保护作用.
这些发现为针对NFE2L2/Nrf2通路的TBI治疗策略提供了理论基础.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.生物信息学是一种生物信息学.细胞内膜网膜应激压力创伤性脑损伤是一种创伤性脑损伤.

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