ApoE靶向NF-κB/p65信号通路在脊髓损伤微环境中的作用与机制研究

The expression of apolipoprotein E (ApoE) can be induced to promote nerve repair after spinal cord injury (SCI), but the mechanism is unknown. Previous studies have shown that, ApoE-KO mice have a significantly higher level of inflammation after SCI, and a significant reduction in behavioral scores compared to wild-type mice. This suggests that ApoE may be associated with post-SCI injury microenvironment inflammatory response and SCI neurological function recovery. At the same time we found that, post-SCI inflammatory-specific signaling pathway NF-κB / p65 was activated. Therefore, we hypothesized that ApoE may target NF-κB / p65 signaling pathway to inhibit inflammation in promoting neurological repair after SCI. In this study, the relationship between ApoE gene and SCI nerve repair and inflammation was determined by gene knockout mice. The relationship between inflammatory response and NF-κB / p65 signaling pathway was elucidated by gene silencing technique. The protective effect of ApoE-activated NF-κB / p65 inflammation-related signaling pathway on neurons after SCI and its molecular mechanism. Therefore, this will provide a new idea for SCI treatment.

脊髓损伤（SCI）后可以诱导载脂蛋白E（apolipoprotein，ApoE）表达量升高促进SCI后神经修复，但机制不明。我们前期研究发现，与野生型小鼠相比，ApoE-KO小鼠SCI后炎症水平显著升高，并且行为学评分明显降低。这提示ApoE可能与SCI后损伤微环境中炎症反应及SCI后神经功能恢复有关。与此同时发现SCI后炎症特异性信号通路NF-κB/p65被激活。因此我们推测：ApoE可能靶向NF-κB/p65信号通路抑制炎症促进SCI后的神经修复。本课题拟通过基因敲除小鼠确定ApoE基因与SCI神经修复与炎症的关系；利用基因沉默技术在体外阐明ApoE所干预的炎症反应与NF-κB/p65信号通路的关系，继而揭示ApoE激活的NF-κB/p65炎症相关信号通路在SCI后对神经细胞的保护作用及其分子机制，为SCI的治疗提供一条新思路。

脊髓损伤（SCI）后可以诱导载脂蛋白E（apolipoprotein，ApoE）表达量升高促进SCI后神经修复，但机制不明。我们前期研究发现，与野生型小鼠相比，ApoE-KO小鼠SCI后炎症水平显著升高，并且行为学评分明显降低。这提示ApoE可能与SCI后损伤微环境中炎症反应及SCI后神经功能恢复有关。与此同时发现SCI后炎症特异性信号通路NF-κB/p65被激活。因此我们推测：ApoE可能靶向NF-κB/p65信号通路抑制炎症促进SCI后的神经修复。本课题拟通过基因敲除小鼠确定ApoE基因与SCI神经修复与炎症的关系；利用基因沉默技术在体外阐明ApoE所干预的炎症反应与NF-κB/p65信号通路的关系，继而揭示ApoE激活的NF-κB/p65炎症相关信号通路在SCI后对神经细胞的保护作用及其分子机制，为SCI的治疗提供一条新思路。