ArticleJournal of translational medicine2025
Micheliolide attenuates sepsis-induced acute lung injury by suppressing mitochondrial oxidative stress and PFKFB3-driven glycolysis.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Targeting mitochondrial apoptosis in septic lung injury: protective potential of omega-3 fatty acids.Apoptosis : an international journal on programmed cell death · 2026Article
- Cumambrin B Alleviates Sepsis-Associated Acute Lung Injury by Activating the Nrf2/HO-1 Pathway.Biomedicines · 2026Article
- Protective Effect of luteolin on CLP-induced Sepsis-associated Encephalopathy via Inhibiting p38 MAPK Signalling in a Rat Model.Molecular neurobiology · 2026Article
- Micheliolide and ACT001 as Covalent Modulators of Inflammation-Redox-Metabolism Networks in CNS Disorders: An Evidence-Stratified Review of Mechanisms and Translational Challenges.Drug design, development and therapy · 2026Review
- Micheliolide reduces the damage, pyroptosis and oxidative stress of cardiomyocytes caused by OGD/R by regulating the AMPK signaling pathway.Journal of clinical biochemistry and nutrition · 2026Article
- Macrophage metabolic reprogramming in sepsis-associated acute lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2026Review
- PFKFB3-Inhibitor 3PO-Mediated Glycolytic Reprogramming Promotes Inflammatory Dental Pulp Repair: An In Vitro and In Vivo Study.International endodontic journal · 2025Article
- Adiponectin pathway regulates cerebral metabolic dysfunction and neuroinflammation via the AdipoR1/PI3K/Akt axis in Perioperative Neurocognitive Disorder.BMC geriatrics · 2025Article
- Oxidative stress in ARDS: mechanisms and therapeutic potential.Frontiers in pharmacology · 2025Review
- SIRT1 Enhancement is Required for the Induction of Anti-Inflammatory Effect of Micheliolide in Carbon Tetrachloride Induced Liver Fibrosis in Mice.Journal of inflammation research · 2025Article
- Protective effects ofFrontiers in nutrition · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundSepsis is a potentially fatal condition with a significant risk of death. Acute lung injury (ALI) is a life-threatening complication of sepsis, and the inflammatory response plays a critical role in sepsis-induced ALI. The protective effects of micheliolide (MCL) against renal fibrosis and leukemia have been demonstrated, but the precise underlying mechanisms remain unclear.
methodsIn vitro, lipopolysaccharides (LPS) and interferon-gamma (IFN-γ) were used to stimulate RAW264.7 cells and bone marrow-derived macrophages (BMDMs) to investigate the protective effect of MCL on sepsis-induced ALI. Cecal ligation and puncture (CLP) models were constructed in mice to induce ALI in vivo. The expression of inflammatory factors, macrophage polarization markers, and the glycolysis-related enzyme 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) were measured in vivo. Mitochondrial function, oxidative stress, and mitochondrial-related proteins were evaluated in vitro.
resultsMCL inhibited CLP-induced ALI, as evidenced by improvements in proinflammatory factor levels, lung wet/dry ratios, and histopathological findings. In vitro, MCL treatment significantly suppressed LPS + IFN-γ-induced M1-type polarization of RAW264.7 cells and BMDMs, as well as the production of inflammatory factors and oxidative stress. Mechanistic experiments revealed that MCL suppresses PFKFB3-driven glycolysis to reduce inflammation and activates the mitochondrial unfolded protein response (UPR
conclusionThis study is the first to demonstrate that MCL attenuates sepsis-induced ALI by reducing M1-type macrophage polarization. Its therapeutic effect is closely related to the suppression of oxidative stress and PFKFB3-driven glycolysis.
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