Inflammatory disorders such as sepsis are a major cause of morbidity and mortality. Mitochondrial dysfunction is considered a key factor in the pathogenesis of severe inflammation. In the present study, we aimed to investigate the impact of arachidonic acid, omega-3 (n-3) fatty acids, and n-3-derived lipid mediators 18R-HEPE and resolvin (Rv) E1 on mitochondrial function in experimental inflammation. The results revealed that, in contrast to n-6 and n-3 fatty acids, both 18R-HEPE and RvE1 possess anti-inflammatory and anti-apoptotic properties. Both mediators are able to restore inflammation-induced mitochondrial dysfunction, which is characterized by a decrease in mitochondrial respiration and membrane potential, as well as an imbalance of mitochondrial fission and fusion. Furthermore, inhibition of mitochondrial fission by Mdivi-1 and Dynasore reduces levels of the pro-inflammatory cytokines IL-6 and IL-8. These results suggest a novel functional mechanism for the beneficial effects of RvE1 in inflammatory reactions.

诸如败血症等炎性疾病是发病率和死亡率的主要原因。线粒体功能障碍被认为是严重炎症发病机制中的关键因素。在本研究中，我们旨在研究花生四烯酸，ω-3（n -3）脂肪酸和n -3-衍生的脂质介体18 R -HEPE和resolvin（Rv）E1对实验性炎症中线粒体功能的影响。结果表明，与n -6和n -3脂肪酸相比，两者的18 R-HEPE和RvE1具有抗炎和抗凋亡特性。两种介体均能够恢复由炎症引起的线粒体功能障碍，其特征在于线粒体呼吸和膜电位的降低，以及线粒体裂变和融合的失衡。此外，Mdivi-1和Dynasore对线粒体裂变的抑制作用会降低促炎细胞因子IL-6和IL-8的水平。这些结果表明RvE1在炎症反应中有益作用的新型功能机制。