阿德罗宾在实验性脑下关节下出血中的保护作用
Ayşenur Sümer Coşkun1, Mehmet Bülbül2, Tuğçe Çeker3
1Division of Anesthesia and Reanimation, Kepez State Hospital, 07320 Antalya, Turkey.
Neuroscience
|June 8, 2024
概括
阿德罗 (AD) 给药改善了神经功能,并减少了大脑损伤在小鼠模型下arachnoid出血 (SAH). 这种增强了抗氧化能力,减少了细胞死亡,提供神经保护.
科学领域:
- 神经科学是一个神经科学.
- 生物化学 生物化学
- 病理学 病理学 病理学
背景情况:
- 下关节下出血 (SAH) 是一种严重的神经疾病,具有显著的发病率和死亡率.
- 在SAH之后的早期脑损伤涉及复杂的病理生理过程,包括氧化应激和亡.
- 针对这些早期机制的治疗策略对于改善患者结果至关重要.
研究的目的:
- 在SAH的老鼠模型中研究外源性给予阿德罗宾 (AD) 的早期神经保护作用.
- 评估AD对神经功能的影响,内皮氧化合成酶 (eNOS) 表达,酸盐/酸盐水平,氧化应激和SAH后的亡.
主要方法:
- 在Sprague-Dawley大鼠中,SAH通过自主血液的脑内静脉注射来诱导.
- 在SAH诱导后,Adropin (AD) 进行了脑内静脉注射.
- 用修改的加西亚分数来评估神经功能.
- 测量了包括eNOS表达,亚酸盐/亚酸盐,总抗氧化能力 (TAC),活性氧/物种 (ROS/RNS) 和caspase-3在内的生化标志物.
- 免疫组织化学被用来检测eNOS表达和亡神经元.
主要成果:
- 与假冒和SAH+AD组相比,SAH大鼠的修改Garcia分数显著较低.
- 阿德罗宾的使用增加了大脑的eNOS表达,酸盐/酸盐和AD水平.
- SAH导致ROS/RNS增加和TAC减少;AD的管理增加了TAC和减少了ROS/RNS.
- 在SAH大鼠中,亡细胞数量和强度增加,但在AD治疗后降低.
结论:
- 在SAH的早期阶段,Adropin (AD) 的使用显著改善了神经功能.
- 阿尔茨海默病治疗增强了eNOS表达,增强了抗氧化能力,并减少了SAH大脑中的氧化应激和亡.
- 这些发现表明,阿德罗可以提供神经保护,防止与下大脑关节出血相关的早期脑损伤.
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