在心脏骤停后,人体血中ROS的持续增加生成通过Amplex Red氧化法确定
Muhammad Shoaib1,2, Nancy Kim1,2, Rishabh C Choudhary1
1Laboratory for Critical Care Physiology, The Feinstein Institutes for Medical Research, Manhasset, NY, USA.
Free radical research
|August 29, 2023
概括
由血生成的活性氧物种 (ROS) 引起的氧化应激可能会对心脏骤停 (CA) 后的患者造成伤害. 这项研究发现CA后人体血ROS增加,表明新的治疗点.
科学领域:
- 生物化学 生物化学
- 心血管研究研究心血管研究
- 氧化压力是一种氧化压力.
背景情况:
- 氧化应激是心脏骤停 (CA) 损伤的重要因素.
- 组织衍生反应性氧物种 (ROS) 的作用已得到充分研究.
- 血产生的ROS对CA病理学的贡献在很大程度上仍未被探索.
研究的目的:
- 研究血作为心脏骤停后ROS生成的来源.
- 量化来自CA患者的人类血样本中的实时ROS生成.
- 探索潜在的治疗策略,以向血衍生的ROS.
主要方法:
- 使用Amplex Red (AR) 试验来测量在隔离的血中实时生成ROS.
- 使用CA后大鼠血来识别和考虑AR氧化中的干扰因素.
- 分析了来自CA患者和对照组的人类血样本,考虑到确定的混因素.
主要成果:
- 在CA后的老鼠血中观察到显著增加的AR氧化率.
- 在大鼠血中最初的发现归因于氧化酶活性,而不是ROS.
- 人类CA患者的血显示ROS生成显著增加,即使在抑制氧化酶的情况下也持续存在.
结论:
- 血是人类心脏骤停后持续产生ROS的重要来源.
- 在CA后血ROS的增加代表了患者受伤的潜在主要原因.
- 针对全身血ROS的抗氧化策略可能会改善患者的治疗结果.
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