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作为NMDA受体抑制剂MK801,缓解了BV-2微质细胞的促炎分化

Chih-Cheng Wu¹, Chung-Yuh Tzeng², Cheng-Yi Chang³

¹Department of Anesthesiology, Taichung Veterans General Hospital, Taichung City, 407, Taiwan; Department of Financial Engineering, Providence University, Taichung City, 433, Taiwan; Department of Data Science and Big Data Analytics, Providence University, Taichung City, 433, Taiwan.

European journal of pharmacology

|July 21, 2023

概括

通过影响线粒体动力学,N-甲基-D-酸盐 (NMDA) 受体促进微质中的炎症. 作为NMDA受体抑制剂的MK801通过阻断这种途径,显示出抗炎作用的潜力,从而提供治疗可能性.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

中枢神经系统的免疫细胞微质表现出受两极分化影响的多种功能.
线粒体对于细胞能量,信号传递和免疫力至关重要,其动态影响细胞功能.
N-甲基-D-酸盐 (NMDA) 类型的谷氨酸受体与神经传递,神经毒性和炎症有关.

研究的目的:

研究NMDA受体和线粒体动态在脂聚糖 (LPS) 诱导的微质激活中的作用.
探索微质中NMDA受体抑制的抗炎潜力.

主要方法:

使用了用LPS刺激的BV-2微质细胞.
检查了蛋白质酸化,细胞内调动和炎症标志物.
评估了线粒体功能障碍指标,包括Dynamin-Related Protein 1 (Drp1) 激活和反应性氧物种 (ROS) 生成.
研究了NMDA受体阻塞 (MK801) 和CaMKII,Drp1和ROS的抑制剂的影响.

主要成果:

LPS刺激激活了NMDA受体,导致CaMKII酸化增加,流入,随后激活了TAK1/NF-κB通路.
LPS诱导了M1的炎症性两极化和细胞因子表达,伴随着线粒体功能障碍 (增加Drp1,NOX2,ROS).
MK801,KN93,Mdivi-1和阿波辛因减弱了LPS诱导的炎症反应和线粒体功能障碍.

结论:

通过线粒体动力学激活NMDA受体,通过CaMKII/Drp1/ROS/NF-κB轴驱动促炎性微质反应.
MK801在抑制微质激活和减轻炎症损伤方面表现出潜力,这表明它是一个治疗点.

关键词:

炎症炎症是一种炎症.线粒体动力学的动态这种NMDA受体是NMDA受体.两极化的偏化

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