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内源性反应性氧物种和氧化在调节缺氧星体中的HIF-1α表达方面具有相反的作用

Qingquan Chen¹, Wenlan Liu¹, Xi Sun¹

¹Department of Pharmaceutical Sciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.

Biophysics reports

|June 8, 2023

概括

缺氧增加缺氧诱导因子 (HIF) 在缺血性中风. 这项研究揭示了氧化 (NO) 和活性氧物种 (ROS) 相互作用以调节HIF-1alpha,而NO有可能平衡ROS介导的压力.

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:

缺血性中风导致大脑缺氧,增加缺氧诱导因子 (HIF) 表达,这是大脑损伤的关键因素.
氧化 (NO) 和活性氧物种 (ROS) 在缺氧/缺血期间都升高,并且独立地影响HIF-1alpha.
了解NO和ROS在脑缺血期间调节HIF-1alpha的相互作用至关重要.

研究的目的:

为了研究NO和ROS对缺氧星球细胞中HIF-1α表达的交叉效应.
在缺血性脑损伤的背景下阐明HIF-1alpha的调节机制.

主要方法:

星球细胞被暴露于低氧2小时.
测量了HIF-1alpha蛋白,NO和ROS的水平.
包括NAC,DPI,MnTMPyP (ROS清除剂),L-NAME (NOS抑制剂) 和PTIO (NO清除剂) 在内的药物剂被用于调节NO和ROS水平.

主要成果:

缺氧显著增加了星球细胞中的HIF-1alpha蛋白,NO和ROS的产生.
减少ROS降低了HIF-1alpha和增加了NO;NOS抑制降低了ROS和HIF-1alpha.
结合的NOS抑制和ROS清除逆转了HIF-1alpha的减少;NO清除增加了HIF-1alpha和ROS,但结合的NO/ROS清除减少了HIF-1alpha.

结论:

ROS,NO和它们的相互作用极大地调节了缺氧诱导的HIF-1alpha蛋白积累.
缺氧诱导的NO可以作为一种内源机制,通过抑制HIF-1alpha积累来平衡ROS介导的缺氧压力.

关键词:

星球细胞是星球细胞.氧气过低是因为缺氧.缺氧诱导因子1 缺氧诱导因素1 氧化氧化是什么?有反应性氧物种的反应性氧物种.

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