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通过诱导自性功能障碍,TSPO会加剧急性脑缺血/再输损伤
Yusufu Mahemuti1, Kaheerman Kadeer2, Riqing Su2
1Department of Neurosurgery, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, Xinjiang, PR China; School of Brain Science and Brain Medicine, Zhejiang University School of Medicine, Hangzhou 310058, Zhejiang, PR China; Liangzhu Laboratory, MOE Frontier Science Center for Brain Science & Brain-Machine Integration, State Key Laboratory of Brain-machine Intelligence, Zhejiang University, Hangzhou 311121, Zhejiang, PR China; NHC and CAMS Key Laboratory of Medical Neurobiology, Zhejiang University, Hangzhou 310058, Zhejiang, PR China.
Experimental neurology
|September 17, 2023
概括
18kDa转位蛋白 (TSPO) 在脑缺血再输液后的中枢神经系统 (CNS) 损伤中起作用. 抑制TSPO可以降低神经炎症,并保护神经细胞,这表明它.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 病理生理学 病理生理学
背景情况:
- 自是一种关键的细胞过程,与中枢神经系统 (CNS) 疾病有关.
- 大脑缺血-反损伤 (CIRI) 涉及中枢神经系统的复杂病理生理变化.
- 18kDa转位蛋白 (TSPO) 参与神经炎症,但其在CIRI中的作用尚不清楚.
研究的目的:
- 调查TSPO在CIRI期间通过微质内自细胞调节神经炎症中的作用.
- 为了确定TSPO是否是缺血性中风的潜在治疗点.
主要方法:
- 在老鼠中利用过渡性中脑动脉封闭 (tMCAO) 和在BV2微质细胞中利用氧-葡萄糖剥夺/氧化 (OGD/R).
- 评估了自标志物 (Beclin-1,LC3B,p62,LAMP-1,Cathepsin-D) 和自流量.
- 测量了反应性氧物种 (ROS) 和促炎因素 (TNF-α,IL-6).
- 采用了共聚焦激光显微镜和传输电子显微镜 (TEM).
主要成果:
- 根据CIRI模型,TSPO表达在大鼠大脑组织和微质细胞中被上调.
- 在CIRI期间,自被过度激活,流动失调.
- 抑制TSPO改善了自细胞过度激活,减少了ROS,并减少了促炎因素.
- 抑制TSPO缓解了微质神经炎症和保护神经细胞.
结论:
- 在CIRI期间,TSPO通过影响微质中的自功能障碍来调节神经炎症.
- 在缺血性中风模型中,TSPO抑制表明神经保护作用.
- TSPO代表了治疗缺血性中风的潜在治疗标.
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