纳托金酶在缺血性中风中的神经保护机制:针对炎症,氧化应激和凝血
Xin-Ying Yang1, Sheng-Lin Wang1, Wen-Chi Xue1
1Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang, China.
Antioxidants & redox signaling
|August 13, 2024
概括
纳托金酶 (NK) 通过减少炎症和氧化应激,显示出对缺血性脑损伤的神经保护作用. 它在中风模型中的治疗效益与其酶活性有关.
科学领域:
- 神经科学是一个神经科学.
- 药理学 药理学是指药理学的学科.
- 生物化学 生物化学
背景情况:
- 纳托金酶 (NK) 是一种血清内酶,在神经再生方面表现有前途.
- 大脑缺血-再输液损伤是神经损伤的重要原因.
研究的目的:
- 调查纳托金酶在短暂中脑动脉阻塞 (tMCAO) 的老鼠模型中的神经保护作用.
- 阐明纳托金酶在脑缺血-再输液损伤中的作用的潜在机制.
主要方法:
- 在tMCAO手术前,每天给老鼠服用不同剂量的Nattokinase.
- 使用体内 (tMCAO) 和体内 (微,OGD/R) 模型评估神经保护.
- 通过蛋白质组分析和使用血清酶内酶抑制剂 (PMSF) 探索了机制.
主要成果:
- 在tMCAO大鼠中,纳托金酶剂量依赖性降低了心脏病发作体积和改善了神经功能.
- NK降低了促炎和凝固细胞因子和减弱的活性氧物种 (ROS).
- 通过调节自,亡和ER压力路径,NK保护神经元免受氧气-葡萄糖剥夺/再输液 (OGD/R) 损伤.
结论:
- 纳托金酶在缺血性脑损伤中表现出多方面的神经保护作用.
- 纳托金酶的治疗疗效取决于它的血清内酶活性.
- 炎症和凝血途径与tMCAO损伤和Nattokinase的治疗作用有关.
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