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阿佩林-13/APJ促进神经干细胞修复缺血性中风

Shuangmei Li¹, Sijun Yuan¹, Shujun Yang¹

¹Department of Emergency, the Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, PR China.

|March 31, 2025

概括

阿佩林-13增强神经干细胞 (NSC) 治疗缺血性中风的功能,通过改善氧气-葡萄糖缺乏 (OGD) 下的细胞活力和迁移. 这种还可以降低细胞亡,并通过APJ受体增强来自大脑的神经营养因子 (BDNF).

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.
药理学药理学是指药理学的学科.

背景情况:

神经干细胞 (NSC) 疗法对缺血性中风有希望,但受到恶劣的缺血和缺氧大脑环境的限制.
正在探索药物刺激策略,以提高NSC在缺血性中风模型中的治疗疗效.

研究的目的:

研究小分子Apelin-13在模拟性缺血条件下改善NSC功能的潜力.
阐明阿佩林-13影响NSC活力,迁移,亡和神经营养因子表达的机制.

主要方法:

神经干细胞接受了氧气-葡萄糖剥夺 (OGD),以模仿缺血病状况.
评估了Apelin-13治疗对NSC活力,迁移和亡的影响.
测量了来自大脑的神经营养因子 (BDNF) 的表达水平.
通过敲击实验,研究了阿佩林-13受体APJ的作用.

主要成果:

阿佩林-13 (100nM) 缓解了OGD诱导的NSC可行性的抑制,并加强了OGD下的NSC迁移.
阿佩林-13降低了OGD诱导的NSC亡,并调节了Bcl-2与Bax的比率.
在OGD条件下,阿佩林-13进一步增加了NSC中的BDNF表达.
抑制APJ受体消除了阿佩林-13在OGD期间对NSC和BDNF表达的有益作用.

结论:

阿佩林-13显著提高NSC活力,迁移和生存,同时在OGD条件下减少细胞亡,通过APJ受体进行介导.
阿佩林-13 / APJ系统,可能通过下游BDNF,代表了一种有前途的治疗策略,以改善基于NSC的缺血性中风治疗方法.
针对Apelin-13/APJ通路可以激活内源性NSC来治疗缺血性中风.

关键词:

申诉人13号的申诉细胞灭亡 (apoptosis) 是一种死亡的过程.这就是为什么BDNF是BDNF.缺血脑卒中脑中风这是一个很好的例子.神经干细胞的神经干细胞

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