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与低剂量胺相比,德克斯梅德托米丁在急性缺血性中风中不仅更好地保护了大脑,而且在急性缺血性中风中更好地保护了肺部

Luciana B B Heil¹, Cassia L Braga¹, Raquel F Magalhães¹

¹Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.

International immunopharmacology

|October 1, 2023

概括

在急性缺血性中风 (AIS) 模型中,德克斯梅托米丁 (DEX) 与低剂量胺 (KET) 相比,在急性缺血性中风 (AIS) 模型中提供更好的神经保护. 在大脑和肺组织中,DEX显著降低了炎症和内皮损伤,这表明了更广泛的治疗益处.

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.
关键护理医学关键护理医学

背景情况:

急性缺血性中风 (AIS) 对大脑和肺功能都有重大风险.
德克斯梅托米丁 (DEX) 和低剂量胺 (KET) 已知在AIS中具有神经保护性.
缺乏对DEX与KET在AIS中保护大脑和肺组织的疗效进行比较的研究.

研究的目的:

在急性缺血性中风 (AIS) 的小鼠模型中,比较德克斯梅德托米丁 (DEX) 和低剂量胺 (KET) 的保护作用.
在AIS之后,评估DEX和KET对大脑和肺组织的影响.
评估DEX和KET对炎症和细胞损伤的保护作用背后的分子机制.

主要方法:

在Wistar大鼠中诱导AIS,然后随机分配给接受DEX或低剂量S(+) - 胺 (KET).
收集了大脑和肺部组织进行组织学和分子分析,包括对亡,炎症标记物 (TNF-α,VCAM-1) 和抗氧化酶 (Nrf2,SOD-1) 的评估.
对膜巨细胞,中性粒细胞和肺内皮细胞的影响是根据特定的细胞标记物和表型来评估的.

主要成果:

虽然亡并没有不同,但与KET相比,DEX治疗显示TNF-α和VCAM-1在脑组织中的表达减少.
在肺组织中,DEX治疗导致TNF-α和VCAM-1的减少,并增加了Nrf2和SOD-1水平.
DEX调节了巨细胞的表型,使其具有抗炎M2特征,并减少了中性粒细胞和内皮细胞中的炎症标志物.

结论:

在AIS模型中,德克斯梅德托米丁与低剂量胺相比,具有更好的保护作用.
在AIS后,DEX有效地减少脑和肺组织中的炎症和内皮细胞损伤.
这些发现表明,DEX作为一种潜在的更有益的治疗剂,用于管理具有多器官保护的AIS.

关键词:

大脑 - 肺相互作用.德克斯梅德米丁的使用方法焦点缺血性中风是因为炎症炎症是一种炎症.胺基氨酸 (ketamine) 是一种可以

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