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在创伤性脑损伤后,uqcr11可缓解氧化应激和亡

Yujian Lin¹, Jingjing Zhang¹, Dongqing Lu¹

¹Department of Human Anatomy, Institute of Neurobiology, Nantong University, No.19 Qixiu Road, No.3 Building of Qixiu Campus, Nantong 226001, Jiangsu, PR China.

Experimental neurology

|October 26, 2023

概括

在创伤性脑损伤 (TBI) 中观察到,乌比金诺-细胞染色体c减少酶,复杂III亚单元XI (Uqcr11) 的表达较低. Uqcr11过度表达保护神经元免受损伤,这表明它是TBI恢复的治疗目标.

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
生物化学生物化学

背景情况:

创伤性脑损伤 (TBI) 是导致死亡和残疾的主要原因.
由于外部物理力量,TBI导致大脑功能障碍.
了解TBI背后的分子机制对于开发有效治疗方法至关重要.

研究的目的:

调查Ubiquinol-cytochrome c减少酶,复杂III亚单元XI (Uqcr11) 在TBI中的作用.
为了确定Uqcr11表达水平是否在TBI中发生变化.
在TBI模型中探索Uqcr11调制的治疗潜力.

主要方法:

在TBI小鼠的大脑皮层中评估Uqcr11表达.
建立了一个体外神经元损伤模型,使用H2O2和缺氧复氧化 (H/R).
在HT22细胞和TBI小鼠中过度表达的Uqcr11,以评估其影响.

主要成果:

在TBI小鼠的大脑皮质中检测到较低的Uqcr11表达.
在实验室中,uqcr11过度表达减弱了H2O2或H/R诱导的神经元损伤.
通过抑制氧化应激和促进神经元存活,uqcr11上调改善了TBI小鼠的运动功能,学习和记忆.

结论:

在TBI中,uqcr11对神经元损伤起着保护作用.
过度表达Uqcr11可以减轻TBI后的氧化应激和神经元亡.
Uqcr11代表了改善TBI结果的潜在治疗标.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.神经行为功能神经行为功能氧化应激是一种氧化应激.创伤性脑损伤是一种创伤性脑损伤.一个Uqcr1111的时间.

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Traumatic Brain Injury l: Introduction

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