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丰富的环境通过SDF-1/CXCR4/AKT/mTOR通路增强缺血性中风中的血管生成

Yonggang Zhang¹, Sheng Qiu¹, Yi Pang²

¹Huzhou Central Hospital, The Fifth School of Clinical Medicine of Zhejiang Chinese Medical University, Huzhou, China; Huzhou Key Laboratory of Basic Research and Clinical Translation for Neuromodulation, Huzhou, China.

Cellular signalling

|October 13, 2024

概括

丰富环境 (EE) 疗法通过通过SDF-1/CXCR4/AKT/mTOR途径促进血管生长 (血管新生) 来改善缺血性中风 (IS) 后的结果.

科学领域:

神经科学是一个神经科学.
再生医学是一种再生医学.
分子生物学分子生物学

背景情况:

环境丰富 (EE) 是一种非药理学方法,促进血管新生,这对于缺血性中风 (IS) 后的恢复至关重要.
通过EE增强老年人后IS血管生成的确切机制尚未完全理解.
研究这些机制对于开发有效的中风恢复治疗策略至关重要.

研究的目的:

阐明通过EE调解老年小鼠在IS之后血管生成的分子途径.
检查SDF-1/CXCR4/AKT/mTOR信号轴在EE诱导的神经保护和血管生成中的作用.
使用体内 (老年IS小鼠) 和体内 (氧气-葡萄糖剥夺/再输液诱导的bEnd.3细胞) 模型验证发现.

主要方法:

在体内研究涉及对12个月大的IS小鼠进行EE治疗,并评估神经缺陷,血管生成标志物和关键信号蛋白.
药理干预包括SDF-1,SDF-1中和抗体,CXCR4抑制剂 (AMD3100),AKT抑制剂 (ARQ092) 和mTOR抑制剂 (拉帕米辛).
在体外实验中使用了接受氧-葡萄糖剥夺/再输液 (OGD/R) 的bEnd.3细胞来评估细胞迁移和通路激活.

主要成果:

在老年IS小鼠中,EE治疗显著改善了神经功能和增强了血管生成.
在EE上调节了流体细胞衍生因子-1 (SDF-1),血管内皮生长因子A (VEGFA),并激活了AKT/mTOR通路.
抑制SDF-1/CXCR4或AKT/mTOR信号消除了EE的有益作用,而外源的SDF-1模仿了EE的保护作用.

结论:

丰富的环境增强了血管生成,并改善了老年小鼠患有缺血性中风的结果.
该SDF-1/CXCR4/AKT/mTOR通路是EE的亲血管和神经保护作用的关键调解者.
准这种途径对中风恢复具有治疗潜力.

关键词:

血管新生的产生.丰富的环境丰富的环境缺血性中风是因为缺血性中风.在 SDF-1/CXCR4/AKT/mTOR 信号通路中.

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