罗夫米拉斯特通过通过Nrf2/STING/NF-κB通路调节微细胞表型,减轻视网膜缺血/再输伤后的神经炎症

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Yuyan Guo¹, Chunlian Ou², Naiyuan Zhang³

¹Department of Ophthalmology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong, China; Department of Ophthalmology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, Guangdong, China.

International immunopharmacology

|September 26, 2023

概括

罗夫米拉斯降低神经炎症,通过转移微质极化,在受伤后保护视网膜细胞. 这种细胞保护作用由Nrf2/STING/NF-κB通路介导,为视觉功能障碍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.
眼科医生眼科眼科
免疫学免疫学免疫学

背景情况:

视网膜缺血/反 (RIR) 导致神经炎症和视网膜质细胞 (RGC) 死亡,导致不可逆转的视力丧失.
异常的微质细胞 (MG) 两极化有助于RIR诱导的神经炎症.
罗夫米拉斯 (Roflu) 正在研究其在神经炎症疾病中的潜在治疗作用.

研究的目的:

研究Roflumilast对RIR诱导的神经炎症的细胞保护作用.
阐明涉及Roflumilast保护机制的潜在信号通路.

主要方法:

在C57BL/6J小鼠和BV2细胞系中进行了实验.
定量实时PCR和ELISA测量了炎症因素.
组织学和免疫光染色评估了视网膜形态,MG和RGC状态.
西方涂抹和全基因组测序分析了Nrf2/STING/NF-κB通路,并确定了改变的分子.

主要成果:

罗夫卢米拉斯特显著减弱了MG激活,并将其表型从促炎M1转变为抗炎M2.
罗夫卢降低了活性氧物种 (ROS) 水平,并增加了抗氧化酶表达 (血红氧酶1,NAD(P) H氨酸氧降解酶1).
神经保护主要通过对Nrf2/STING/NF-κB通路的调高来调节,而Nrf2抑制则取消了效果.

结论:

罗夫米拉斯通过促进M2 MG极化来抑制RIR诱导的神经炎症.
该机制涉及Nrf2/STING/NF-κB通路的上调.
罗夫米拉斯特证明了对RIR诱导的视觉功能障碍的治疗潜力.

关键词:

微质细胞是微质细胞.这是神经炎症性.Nrf2/STING/NF-κBB 在线播放视网膜缺血/再输血视网膜缺血/再输血罗夫卢米拉斯的最后一个.

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