同类氨酸诱导大脑和视网膜微血管内皮细胞屏障损伤和通过NLRP3炎症酶途径通过差异性超透性
O'lisa Yaa Waithe1, Aliyah Anderson1, Saravanakumar Muthusamy1
1Department of Surgery and Neuroscience Institute, Morehouse School of Medicine, Atlanta, Georgia, USA.
概括
同类氨酸 (HCY) 增加了血视网膜和血脑屏障的透性. NLRP3炎症体起着作用,特别是在大脑内皮细胞中,这表明SANS等疾病的治疗点.
科学领域:
- 神经科学是一个神经科学.
- 眼科医生 眼科 眼科
- 血管生物学 血管生物学
背景情况:
- 同型氨酸 (HCY) 与神经眼综合征 (如SANS) 有关.
- 血视网膜屏障 (BRB) 和血脑屏障 (BBB) 功能障碍是SANS的关键.
- 在SANS病理生物学中HCY和NLRP3炎症酶的作用需要研究.
研究的目的:
- 为了研究同类氨酸 (HCY) 如何影响BRB和BBB的透性.
- 确定NLRP3炎症酶在HCY诱导的屏障功能障碍中的作用.
- 评估SANS.的潜在治疗点.
主要方法:
- 人类大脑和视网膜的微血管内皮细胞 (HBMEC和HRMEC) 用HCY进行治疗.
- 用NLRP3炎症酶抑制剂MCC950来评估其调节作用.
- 试验包括细胞活力,酶-1活性,ZO-1表达和屏障透性.
主要成果:
- 在视网膜和大脑内皮细胞中,HCY显著增加了超透性.
- 在大脑内皮细胞中,MCC950减弱了HCY诱导的超透性.
- HCY增加了caspase-1活性,并改变了紧结蛋白ZO-1的表达.
结论:
- 在视网膜和大脑内皮细胞中,HCY诱导了超透性.
- 在脑内皮细胞中,NLRP3炎症酶介导的效应更为明显.
- 这些发现突显了HCY和NLRP3在SANS相关的屏障功能障碍中的参与.
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