ArticlePloS one2024
Sivelestat improves acute lung injury by inhibiting PI3K/AKT/mTOR signaling pathway.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Extracellular vesicle-mediated mechanisms and therapeutic potential in acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Sivelestat sodium alleviates sepsis-associated acute lung injury by inhibiting ferroptosis via the Nrf2/SLC7A11/GPX4 axis.PloS one · 2026Article
- Natural products in treating sepsis-associated lung and liver injuries by mediating ferroptosis, current progress, and future perspective.Frontiers in pharmacology · 2026Review
- Research on the process and molecular mechanism of inhibiting serous ovarian cancer by PRTN3 and its inhibitor Sivelestat.Journal of ovarian research · 2025Article
- Trans-Sodium Crocetinate Ameliorates High-Altitude Acute Lung Injury via Modulating EGFR/PI3K/AKT/NF-κB Signaling Axis.Nutrients · 2025Article
- Effect of sivelestat on postoperative outcomes in patients with acute type A aortic dissection and hypoxemia: a retrospective analysis.American journal of cardiovascular disease · 2025Article
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8 authors.
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Abstract
objectiveTo investigate the therapeutic effect and mechanism of sivelestat sodium on acute lung injury (AIL).
methodsA rat model for ALI/acute respiratory distress syndrome (ALI/ARDS) was established. Pathological examination of lung tissue was conducted to assess lung injury. Blood gas in the arteries was measured using a blood analyzer. Changes in PaO2, PaO2/FiO2, and lung wet/dry (W/D) weight ratio were carefully compared. ELISA assay was conducted to estimate cell adhesion and inflammation response. Finally, real-time reverse transcription polymerase chain reaction and western blotting assay was used to determine the activation of PI3K/AKT/mTOR pathway.
resultsARDS in vivo model was successfully constructed by LPS injection. Compared with the sham group, PaO2 and PaO2/FiO2 were significantly lower in the vehicle group, while the lung W/D ratio, the lung injury score, NE, VCAM-1, IL-8 andTNF-αwere significantly increased. After treatment with different doses of sivelestat sodium, we found PaO2, PaO2/FiO2 were prominently increased, while the lung W/D ratio, the lung injury score, NE, VCAM-1, IL-8, TNF-α levels were decreased in the dose-dependent manner. Meanwhile, compared with the vehicle group, the expression levels of Bax, PI3K, Akt and mTOR were significantly lower, and the expression of Bcl-2 was significantly higher after injection with sivelestat sodium.
conclusionSivelestat sodium has an interventional effect on ALI in sepsis by inhibiting the PI3K/AKT/mTOR signalling pathway.
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