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吗啡预约缓解缺血/再输液诱导的卡斯巴-8依赖的神经细胞亡通过cPKCγ-NF-κB-cFLIP L路径

Yaru Huang¹, Wenying Chi¹, Yan Li¹

¹Department of Anesthesiology, Central Hospital Affiliated to Shandong First Medical University, Shandong, PR China.

Journal of neurosurgical anesthesiology

|April 5, 2024

概括

吗啡预条件 (MP) 通过减少神经元亡来保护大脑免受缺血/再输的脑损伤. 这种神经保护通过cPKCγ-NF-κB-cFLIP L通路发生,抑制Caspase 8.

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
药理学药理学是指药理学的学科.

背景情况:

外科手术期间的大脑缺血症/再输液损伤是死亡率和认知能力下降的重要原因.
吗啡预调 (MP) 显示出模仿抗缺血/再输伤害保护预调的潜力.
通过MP缓解缺血症/再输液诱导的神经细胞亡的确切机制仍然不完全理解.

研究的目的:

阐明吗啡预条件 (MP) 在防止大脑缺血/再输 (I/R) 损伤的基础分子机制.
研究MP在I/R之后调节神经元亡中的作用.
为了确定MP介导的神经保护所涉及的特定信号通路.

主要方法:

已建立的中脑动脉封闭/再输的小鼠模型 (MCAO/R) 和氧气-葡萄糖剥夺/再氧化 (OGD/R) 的初级皮质神经元模型.
在体内评估神经学缺陷,心脏病发作大小和蛋白质表达 (西部斑).
在试验室中评估了神经元活力 (CCK-8),亡 (TUNEL染色) 和分子标记物 (西部斑,RT-qPCR,免疫光).

主要成果:

在MCAO/R小鼠中,MP显著改善了神经功能,并减少了心脏病发作的大小.
在接受MCAO/R.R.治疗的小鼠中,MP降低了分裂酶-3水平.
通过调节cPKCγ,p-p65,cFLIP L和分裂-caspase-8表达,MP缓解了OGD/R诱导的神经细胞亡.

结论:

吗啡预约有效缓解缺血症/再输液诱导的神经元亡.
MP的保护作用取决于Caspase 8.
MP通过cPKCγ-NF-κB-cFLIP L信号通路发挥其神经保护作用.

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