ArticleScientific reports2026
Sivelestat sodium mitigates lung injury post-acute pulmonary embolism by inhibiting NE-SPP1 neutrophil recruitment and restoring redox balance.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Acute pulmonary embolism (APE) is a major cardiovascular cause of death, characterized by inflammation and oxidative lung injury, for which targeted therapies are lacking. This study investigated the therapeutic potential of Sivelestat sodium, a neutrophil elastase (NE) inhibitor, in a rabbit APE model. APE rabbits were treated with Sivelestat sodium. Cardiopulmonary function was assessed via echocardiography and blood gas analysis. Histopathology, molecular assays (Western blot, RT-qPCR, immunofluorescence), and bioinformatics analysis were used to evaluate injury, inflammation, fibrosis, and the role of secreted phosphoprotein 1 (SPP1). Sivelestat sodium significantly improved cardiopulmonary function and reduced lung damage, neutrophil infiltration, and NETosis. It decreased levels of NE, proinflammatory cytokines (IL-1β, TNF-α, IL-6, IL-8), and markers of coagulation. Treatment also attenuated fibrosis and endothelial barrier injury. Bioinformatics identified SPP1 as a key ECM-related gene. Sivelestat inhibited NE-mediated upregulation of SPP1, subsequently restoring the expression of antioxidant genes (GSTM2, GCLC, GPX1, GPX7) and reducing oxidative stress and collagen deposition. Sivelestat sodium alleviates APE by inhibiting the NE-SPP1 axis, thereby reducing inflammation, oxidative stress, fibrosis, and endothelial injury. This identifies SPP1 as a novel therapeutic target for APE treatment.
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