苏尔福拉阻碍了在极化M1 (LPS) 巨中线粒体重编程和基因素乙化
Sheyda Bahiraii1, Martin Brenner2, Wolfram Weckwerth3
1Department of Pharmaceutical Sciences, University of Vienna, Vienna, Austria; ViennaDoctoral School of Pharmaceutical, Nutritional and Sport Sciences (VDS PhaNuSpo), University of Vienna, Vienna, Austria.
Free radical biology & medicine
|February 1, 2024
概括
硫福拉 (Sfn) 通过维持TCA循环和OXPHOS.维护M1巨细胞中的线粒体功能. 这种新陈代谢重编程限制了乙-CoA,减少了促炎性基因表达.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 代谢过程中的代谢.
背景情况:
- M1巨体表现出促炎特征和变化的新陈代谢,包括增加的糖解和受损的氧化酸化 (OXPHOS).
- 线粒体功能障碍和反应性氧物种 (ROS) 是M1极化的标志.
研究的目的:
- 为了研究硫福拉 (Sfn) 在M1巨分化期间对线粒体重编程的影响.
- 为了确定Sfn介导的线粒体变化如何有助于抑制M1标记物表达.
主要方法:
- 细胞外流量分析,代谢物测定,免疫染和光染料染色.
- 分析线粒体形态,膜潜力和超氧化物生产.
- 颜色测量试验,免疫阻塞和ChIP-qPCR用于素乙化和基因表达.
主要成果:
- 与对照M1细胞相比,Sfn治疗的M1巨细胞保持了完整的TCA循环,更高的OXPHOS,并减少了线粒体ROS.
- 持续的OXPHOS和TCA活性对于减少M1标记基因 (nos2,il1β,il6,tnfα) 是至关重要的.
- 斯芬治疗降低了核乙-CoA水平,导致炎症促进基因促进体的基因乙化减少.
结论:
- 硫福拉在LPS刺激的巨细胞中保留了线粒体的功能.
- Sfn限制了核乙-CoA的可用性,从而抑制了基因素乙化和M1标记基因表达.
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