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在大鼠中,SIRT6的化会在脑缺血-再输血过程中加剧神经元损伤

Bingnan Guo¹, Bin Ma², Ming Li³

¹The Laboratory of Emergency Medicine, School of Second Clinical Medicine, Xuzhou Medical University, Xuzhou, Jiangsu, 221002, China; Department of Emergency Medicine, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, 221002, China.

Nitric oxide : biology and chemistry

|October 7, 2024

概括

化SIRT6降低其活性,在缺血性中风后恶化大脑损伤. 抑制化通过恢复SIRT6功能来保护神经元,为中风提供潜在的治疗点.

科学领域:

神经科学是一个神经科学.
生物化学生化学
病理学病理学病理学

背景情况:

缺血性中风会导致严重的死亡和残疾.
神经元氧化合成酶 (nNOS) 激活和随后的氧化 (NO) 生产加剧脑缺血再注射损伤.
SIRT6对于调节细胞命运至关重要,但其在缺血性中风中的作用尚不清楚.

研究的目的:

调查SIRT6化在脑缺血再注射损伤中的作用.
探索调节SIRT6化的治疗潜力.

主要方法:

使用了四动脉脑缺血再注射的老鼠模型.
评估SIRT6化水平,酶活性和下游分子功能 (PARP1,GCN5).
研究了NMDA受体对抗剂,nNOS抑制剂和白醇的作用.
在SIRT6中进行了位点定向突变发生 (Tyrosine 257到Phenylalanine),并在缺氧-葡萄糖 (OGD) 条件下进行了测试.

主要成果:

增加的SIRT6化减少了它的活性,在缺血性中风模型中恶化了海马神经元损伤.
减少SIRT6化增加了它的活性,并减轻了神经元损伤.
SIRT6化影响了下游的PARP1和GCN5活动,促进了缺血性损伤.
MK801,7-NI和白醇治疗减少了SIRT6化和保护神经元.

结论:

氨酸化SIRT6会损害其酶活性,从而导致缺血性中风中神经元受损.
调节SIRT6化,特别是Tyrosine 257,是脑缺血性疾病的一种有前途的治疗策略.
准NMDA受体,nNOS或氧化应激可以减轻SIRT6化和神经元损伤.

关键词:

大脑缺血-再输血神经元受损的情况.氧化氧化是什么?过氧化酸盐的过氧酸盐关于SIRT6活动的SIRT6活动在SIRT6中化.

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