黑色素通过诱导自减轻大脑缺血症/再输液损伤通过诱导自
Umit Yilmaz1, Kevser Tanbek1, Semir Gul2
1Department of Physiology, Faculty of Medicine, Inonu University, Malatya, Turkey.
Neuroendocrinology
|June 15, 2023
概括
脑缺血 (CI) 后的黑素治疗减少了脑梗塞的大小,并通过调节自和亡来改善神经功能. 这种神经保护作用从受伤后的第五天开始被观察到.
科学领域:
- 神经科学是一个神经科学.
- 生物化学 生物化学
- 药理学 药理学是指药理学的学科.
背景情况:
- 大脑缺血 (CI) 是神经元损伤和死亡的主要原因.
- 自在缺血损伤后的神经元生存中起着复杂的作用.
- 黑色素是一种具有已知的抗氧化和抗炎性能的激素.
研究的目的:
- 调查黑激素给药对CI后自和神经元存活率的影响.
- 为了确定黑激素对神经缺陷得分和运动功能测试的影响.
- 评估黑素对特定的自相关蛋白质 (Beclin-1,LC3,p62) 和亡 (caspase-3) 的影响.
主要方法:
- 使用了一种小鼠模型的焦点脑缺血 (中脑动脉封闭).
- 鼠在输血后的3天或7天内接受了黑激素 (10毫克/公斤/天).
- 进行了神经缺陷,旋转棒和粘合物去除测试.
- 分析了心脏病发作的体积,蛋白质水平 (西方斑,免疫光) 和神经元损伤 (TEM).
主要成果:
- 黑色素治疗显著减少了心脏病发作区域,并从第5天开始改善了运动功能测试的表现.
- Melatonin 上调自蛋白 (Beclin-1, LC3, p62) 和 下调裂开的 caspase-3.
- 传输电子显微镜揭示了半阴影区域神经元损伤的部分减少.
结论:
- 梅拉托尼在CI后的使用表明通过减少心脏病发作的大小和改善功能结果,具有神经保护作用.
- 黑色素调节自和抑制亡,有助于神经元的生存.
- 黑色素的功能益处从脑缺血后的第五天开始显而易见.
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