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针对p38MAPK/NF-κB通路的老化剂和老化物保护内皮细胞免受氧化压力介导的过早衰老

Jingyuan Ya¹, Ulvi Bayraktutan¹

¹Academic Stroke, Mental Health and Clinical Neurosciences, School of Medicine, University of Nottingham, Nottingham NG7 2UH, UK.

|August 9, 2024

概括

准p38MAPK/NF-κB通路和衰老细胞可以保护血脑屏障 (BBB) 免受氧化应激. 这项研究表明,抑制这些途径会延迟内皮细胞衰老,并保持BBB功能.

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
生物化学生物化学

背景情况:

氧化压力导致大脑微血管内皮细胞 (BMEC) 的过早衰老.
这种衰老导致血脑屏障 (BBB) 功能障碍,影响神经健康.
了解这一过程背后的机制对于制定保护策略至关重要.

研究的目的:

调查针对p38MAPK/NF-κB通路和/或衰老细胞是否可以在人类BBB模型中预防氧化应激诱导的衰老.
评估这些干预措施对BBB完整性和功能的保护作用.

主要方法:

使用BMECs,星细胞和周细胞的体外人类BBB模型暴露于过氧化 (H2O2).
通过增加β-galactosidase活性,γH2AX染色,p16表达和管管生成能力受损来确定衰老.
干预措施包括p38MAPK抑制 (BIRB796),NF-κB抑制 (QNZ) 和衰老细胞消除 (达沙替尼/奎尔).

主要成果:

氧化应激诱导了BMECs的过早衰老,损害了BBB完整性 (电阻降低,细胞流量增加).
衰老破坏了紧结蛋白,增加了矩阵金属蛋白酶-2活性,并增加了促炎性细胞因子的释放.
抑制p38MAPK/NF-κB和消除衰老细胞减弱了衰老标志物,减少了炎症,恢复了紧密的结节,并改善了BBB功能.

结论:

针对p38MAPK/NF-κB通路和衰老细胞提供了一个有希望的治疗策略.
缓解这些因素可以保护大脑血管系统免受氧化应激诱导的BBB功能障碍.
这些发现对治疗与BBB分解相关的神经疾病有意义.

关键词:

在 NF-κBB 中.年龄的年龄年龄的年龄.衰老的衰老衰老的衰老血脑屏障血脑屏障血脑屏障血脑屏障细胞内皮细胞的内皮细胞.p38MAPKKK 在线阅读衰老是一种老化.一个老年化的老年主义者.这是一个senomorphic senomorphic.这是一种疗法, senotherapeutic.

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