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吸入的氧化可以抑制实验性缺血性中风中的神经炎症

Rebecca I Sienel¹, Uta Mamrak¹, Janina Biller¹

¹Institute for Stroke and Dementia Research, Klinikum der Universität München and Ludwig Maximilian University (LMU) Munich, Feodor-Lynen Str. 17, 81377, Munich, Germany.

Journal of neuroinflammation

|December 16, 2023

概括

在患有缺血性中风的小鼠中,吸入氧化 (NO) 治疗减少了血管功能障碍和神经炎症. 恢复氧化使血管功能正常,减少炎症标志物并改善结果.

科学领域:

神经科学是一个神经科学.
心血管科学心血管科学
免疫学免疫学免疫学

背景情况:

缺血性中风是全球死亡率和残疾的主要原因.
脑卒中涉及急性血管功能障碍和神经炎症,但它们之间的关系尚不清楚.
氧化 (NO) 在血管健康中起着至关重要的作用.

研究的目的:

调查恢复血管氧化 (NO) 功能是否可以减轻中风后的神经炎症.
为了确定血管功能障碍和缺血性中风中的炎症过程之间的联系.

主要方法:

在实验中,小鼠接受了缺血性中风.
吸入性氧化 (iNO) 治疗是在再输血后进行的.
测量了血管功能标记物 (cGMP,ICAM-1),白细胞粘附和炎症性细胞因子 (IL-1β,IL-6,TNF-α).

主要成果:

iNO使血管循环瓜诺辛单酸盐 (cGMP) 水平正常化.
iNO减少了细胞间粘附分子-1 (ICAM-1) 的表达,并使白细胞粘附正常化.
血管病理的减少与大脑辅酶性炎症性细胞因子的减少相关.

结论:

血管功能障碍驱动白细胞粘附和随后的脑膜炎症在缺血性中风后.
恢复血管NO功能是减少神经炎症的潜在治疗策略.
这种方法也可能有利于其他缺血性疾病.

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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...