ArticleBMC pulmonary medicine2024
Ciprofol prevents ferroptosis in LPS induced acute lung injury by activating the Nrf2 signaling pathway.
Article in BMC pulmonary medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- The Gut Microbiota-Ferroptosis Axis: Emerging Perspectives in Gastrointestinal Tumorigenesis and Progression.Current issues in molecular biology · 2025Review
- Alveolar epithelial cells in bacterial sepsis-associated acute lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundPatients who suffered from sepsis-induced acute lung injury (ALI) always need sedation for mechanical ventilation in intensive care unit (ICU). Ciprofol(Cip), a novel intravenous anesthetic, was revealed to have anti-inflammatory and antioxidative properties. Ferroptosis, categorized as a type of newly non-apoptotic cell death, participates in the development of lung injury. This study aimed to identify the effect of ciprofol on sepsis-induced ALI and to determine whether ferroptosis is involved. METHODS AND
resultsTo create ALI models, MLE12 alveolar epithelial. Cells and lipopolysaccharide (LPS)-stimulated C57BL/6J mice were used. Our results displyed that Cip reduced lung injury and ferroptosis. In the LPS-induced sepsis mice model, Cip pretreatment partially reduced respiratory system damage, as evaluated by HE, TUNEL and inflammatory factors. By raising GSH levels, ciprofol activated the Nrf2 antioxidative pathway, blocked ferroptosis, increased ferroptosis-related protein (GPX4 and SLC7A11) expressions, and reduced Fe
conclusionOur study demonstrated that Cip may prevent septic lung injury by suppressing ferroptosis through the Nrf2 pathway.
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