酸通过上调SOCS3的调节来抑制炎症
Amina Khatun1, Surendra Patra1, Susovon Chowdhury1
1Biodiversity and Environmental Studies Research Centre Affiliated to Vidyasagar University, Paschim Medinipur, West Bengal 721101, India; Department of Biological Sciences, Midnapore City College, Kuturiya, Bhadutala, Paschim Medinipur, West Bengal 721129, India.
Journal of neuroimmunology
|November 22, 2025
概括
酸 (SA) 通过激活CREB.提升微质细胞中的抗炎蛋白SOCS3,从而激活CREB. 这表明,SA可以通过减少炎症分子和活性氧物种来治疗神经炎症性疾病.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
背景情况:
- 微质在神经炎症中起着至关重要的作用.
- 细胞因子信号传递3抑制剂 (SOCS3) 是微质中炎症分子的关键抑制剂.
- 神经炎症与各种神经系统疾病有关.
研究的目的:
- 研究酸 (SA) 对微质细胞中SOCS3表达的作用.
- 阐明SA影响SOCS3水平的机制.
- 评估SA在神经炎症中的潜在治疗应用.
主要方法:
- 用SA治疗N-9小鼠微质细胞和初级微质细胞/星细胞.
- 用脂聚糖 (LPS) 刺激诱导炎症.
- 对SOCS3mRNA和蛋白质水平的分析.
- 测量促炎媒介物 (TNFα,IL1R1,IL1β,iNOS) 和活性氧物种 (ROS).
- 使用siRNA倒置研究cAMP反应元素结合蛋白 (CREB) 的作用.
主要成果:
- 在微质细胞中,SA选择性地以剂量和时间依赖的方式增加了SOCS3水平.
- 治疗SA抑制了LPS诱导的促炎媒介和ROS生成.
- SA增强了-CREB表达,而CREB敲击取消了SA诱导的SOCS3上调.
- 亚胺氨酸证明了对微质中LPS诱导的炎症反应的保护作用.
结论:
- 酸激活CREB,导致微质细胞中SOCS3的表达增加.
- 通过抑制促炎媒介和ROS,SA有效降低神经炎症.
- 在治疗神经炎症性疾病方面,SA显示出治疗潜力.
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