VDR激活通过上调TREM2转录来改善间歇性缺氧相关的认知障碍
Jiahuan Xu1, Hongyu Jin1, Hui Shen1
1Institute of Respiratory and Critical Care Medicine, The First Hospital of China Medical University, Shenyang, China.
用酸醇激活维生素D受体 (VDR) 通过促进TREM2表达,减少神经炎症和神经元损伤来缓解阻塞性睡眠呼吸暂停的认知障碍.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 内分泌学 在内分泌学.
背景情况:
- 阻塞性睡眠呼吸暂停 (OSA) 的间歇性缺氧 (IH) 会导致神经炎症和认知障碍.
- 维生素D受体 (VDR) 激活在治疗其他疾病中的神经炎症和神经元损伤方面表现有前途.
研究的目的:
- 调查VDR激活是否可以减轻与OSA相关的认知障碍.
- 阐明VDR影响OSA中神经炎症和神经元损伤的机制.
主要方法:
- 使用小鼠模型和BV2微质细胞暴露于IH.
- 服用酸盐来激活VDR,并评估其对TREM2表达,微质偏振,神经炎症和神经元损伤的影响.
- 进行TREM2敲击实验以确认其作用.
- 在HEK293T细胞中的TREM2促进体上确定了VDR结合位.
主要成果:
- 卡尔西醇治疗增强了髓状细胞2 (TREM2) 表达的触发受体,并促进了M2微质的两极分化.
- 通过卡尔西醇激活VDR缓解了IH诱导的神经炎症和神经元损伤.
- TREM2的倒置减弱了酸的有益作用.
- 发现VDR与TREM2促进体区域结合,增强其转录.
结论:
- VDR激活改善了在OSA中IH诱导的认知障碍.
- 该机制涉及VDR与TREM2促进器结合,增加TREM2转录,促进M2微质偏振,并减少神经炎症.
- 针对VDR可能为OSA患者的认知缺陷提供治疗策略.
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