诺伯基宁通过抑制NFκB,MAPK和STAT3激活和阻断代谢重编程来预防巨细胞中LPS诱导的炎症反应
Wan Li1,2, Zhengnan Cai1,2, Florian Schindler1,3
1Molecular Systems Biology (MOSYS), Department of Functional and Evolutionary Ecology, University of Vienna, Vienna, Austria.
Frontiers in immunology
|May 30, 2023
概括
诺伯基宁是一种天然化合物,通过抑制关键信号通路和巨细胞中的代谢变化,有效减少炎症. 这为治疗与炎症相关的慢性疾病和癌症提供了一个有希望的替代方案.
科学领域:
- 生物化学 生物化学
- 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:
- 炎症是慢性疾病和癌症的主要驱动因素.
- 现有的抗炎药物由于副作用而受到限制.
- 诺伯基宁是传统抗炎药物的组成部分.
研究的目的:
- 为了研究诺伯热宁对脂聚糖 (LPS) 诱导的巨细胞炎症的预防作用.
- 通过整合代谢学和蛋白质学阐明诺伯热宁抗炎作用的分子机制.
主要方法:
- 利用高分辨率质谱测量用于定量蛋白质组学,识别了近3000种蛋白质.
- 分析差异表达蛋白质以了解分子变化.
- 综合代谢学和蛋白质学数据来探索细胞重编程.
主要成果:
- 诺伯格宁减轻了LPS诱导的氧化 (NO),中白素-1β (IL1β),瘤坏死因子-α (TNFα),中白素-6 (IL6) 和可诱导的氧化合成酶 (iNOS) 的产生.
- 诺伯格宁抑制了NFκB,MAPK和STAT3信号通路的托尔类受体2 (TLR2) 介导激活.
- 诺伯基宁逆转了LPS诱导的代谢重编程,包括抑制糖解,促进氧化酸化 (OXPHOS),并恢复了三碳酸 (TCA) 循环.
结论:
- 诺伯格宁通过调节巨细胞中的炎症信号通路,表现出显著的抗炎作用.
- 诺伯基宁有效地准与炎症相关的代谢重编程.
- 这些发现凸显了诺伯格宁作为治疗炎症状况的治疗剂的潜力.
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