deoxyelephantopin has been researched along with Sepsis* in 2 studies
2 other study(ies) available for deoxyelephantopin and Sepsis
| Article | Year |
|---|---|
Deoxyelephantopin alleviates lipopolysaccharide-induced septic lung injury through inhibiting NF-ĸB/STAT3 axis.
Topics: Anti-Inflammatory Agents; Endothelial Cells; Humans; Lactones; Lipopolysaccharides; Lung Injury; NF-kappa B; Poly(ADP-ribose) Polymerase Inhibitors; Sepsis; Sesquiterpenes; STAT3 Transcription Factor | 2022 |
Deoxyelephantopin decreases the release of inflammatory cytokines in macrophage associated with attenuation of aerobic glycolysis via modulation of PKM2.
Growing evidence suggests that activated immune cells undergo metabolic reprogramming in the regulation of the innate inflammatory response. Remarkably, macrophages activated by lipopolysaccharide (LPS) induce a switch from oxidative phosphorylation to aerobic glycolysis, and consequently results in release of proinflammatory cytokines. Pyruvate Kinase M2 (PKM2) plays a vital role in the process of macrophage activation, promoting the inflammatory response in sepsis and septic shock. Deoxyelephantopin (DET), a naturally occurring sesquiterpene lactone from Elephantopus scaber, has been shown to counteracts inflammation during fulminant hepatitis progression, but the underlying mechanism remains unclear. Here, we studied the function of the DET on macrophage activation and investigated the anti-inflammatory effects of DET associated with interfering with glycolysis in macrophage. Our results first demonstrated that DET attenuates LPS-induced interleukin-1β (IL-1β) and high-mobility group box 1 (HMGB1) release in vitro and in vivo and protected mice against lethal endotoxemia. Furthermore, DET decreased the expression of pyruvate dehydrogenase kinase 1 (PDK1), glucose transporter 1(GLUT1), lactate dehydrogenase A (LDHA), and reduced lactate production dose-dependently in macrophages. Moreover, we further revealed that DET attenuates aerobic glycolysis in macrophages associated with regulating the nuclear localization of PKM2. Our results provided a novel mechanism for DET suppression of macrophages activation implicated in anti-inflammatory therapy. Topics: Aerobiosis; Animals; Anti-Inflammatory Agents; Cytokines; Disease Models, Animal; Glycolysis; Humans; Inflammation Mediators; Lactones; Lipopolysaccharides; Macrophages; Male; Mice; Mice, Inbred C57BL; Pyruvate Kinase; RAW 264.7 Cells; Sepsis; Sesquiterpenes; Signal Transduction | 2020 |