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向JAK2-STAT3通路以抑制cGAS-STING激活可以改善缺血性中风后的神经元衰老

Wei Zhang¹, Meijie Xu¹, Fangyu Chen¹

¹Department of Neurology, Tianjin Medical University General Hospital, Tianjin Neurological Institute, Key Laboratory of Post Neurotrauma, Neurorepair, and Regeneration in Central Nervous System, Ministry of Education and Tianjin City, Tianjin, China.

Experimental neurology

|July 7, 2023

概括

抑制JAK2 / STAT3通路可以减少缺血性中风后的大脑炎症和衰老. 这种使用AG490的方法针对cGAS/STING/NF-κB通路,为中风恢复提供了潜在的治疗方法.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
病理学病理学病理学

背景情况:

脑性缺血后的神经炎症有助于缺血性中风后脑损伤的进展.
简氏激酶2/信号转换器和转录3 (JAK2/STAT3) 激活器通路对于神经炎症至关重要,但其在中风后大脑衰老中的作用尚不清楚.

研究的目的:

研究JAK2/STAT3途径在缺血性中风后大脑衰老中的作用.
评估抑制JAK2/STAT3在缓解中风诱导的大脑损伤和衰老方面的治疗潜力.

主要方法:

使用C57BL/6小鼠模型的缺血性中风.
用一个JAK激酶抑制剂 (AG490) 治疗中风小鼠.
评估了神经行为结果,脑梗塞量,促炎性细胞因子表达,微质激活,氧化DNA损伤和细胞衰老.
研究了循环GMP-AMP合成酶 (cGAS),干扰素基因刺激剂 (STING) 和NF-κB p65.5的表达.

主要成果:

在中风小鼠中,AG490治疗改善了神经行为功能,并减少了脑梗塞体积.
AG490降低了促炎性细胞因子表达和微质激活.
用AG490治疗减少了氧化DNA损伤和细胞衰老.
AG490 抑制了cGAS,STING 和NF-κB p65.5 的表达.

结论:

抑制JAK2/STAT3通路可以缓解缺陷神经和脑损伤后缺血性中风.
抑制JAK2/STAT3的治疗效果很可能是通过抑制cGAS/STING/NF-κB p65通路,减少神经炎症和神经元衰老.
向JAK2/STAT3通路为预防衰老和改善缺血性中风后的结果提供了一个有希望的治疗策略.

关键词:

细胞衰老细胞衰老缺血性中风是因为缺血性中风.神经炎症是一种神经炎症.神经功能障碍的神经功能障碍氧化应激是一种氧化应激.

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相关概念视频

The JAK-STAT Signaling Pathway

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...