ArticleMolecular biology reports2026
1,25(OH)₂D₃ mitigates bronchopulmonary dysplasia via modulation of the TXNIP-NLRP3-GSDMD signaling pathway.
Article in Molecular biology 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
backgroundBronchopulmonary dysplasia (BPD) is a chronic lung disease associated with preterm birth. Vitamin D (VitD) is essential for lung development and maturation.
objectiveTo investigate the protective effects of 1,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃] on BPD and explore its potential mechanisms, focusing on the TXNIP-NLRP3-GSDMD inflammatory signaling pathway.
methodsA hyperoxia-induced BPD model was established in Sprague-Dawley rats. Primary alveolar type II epithelial cells (AEC IIs) were exposed to normoxia or hyperoxia with or without 1,25(OH)₂D₃ and lipopolysaccharide (LPS), which was used as a general inflammatory stimulus. Lung histology and ultrastructure were evaluated by H&E staining and transmission electron microscopy. Oxidative stress, inflammatory responses, and protein expression were assessed by immunofluorescence, RT-qPCR, ELISA, and western blotting. Cell viability and oxidative status were analyzed using CCK-8, EdU, MDA, and SOD assays.
results1,25(OH)₂D₃ improved AEC II viability and proliferation, reduced MDA levels (P < 0.05), and increased SOD activity (P < 0.05) under hyperoxic conditions. In addition, 1,25(OH)₂D₃ decreased inflammatory cytokine levels (IL-1β, IL-18, IL-6, IL-33, TNF-α) (P < 0.05) and reduced expression of proteins associated with the TXNIP-NLRP3-GSDMD pathway, which has been implicated in pyroptosis. Lung injury and alveolar simplification were alleviated following 1,25(OH)₂D₃ treatment. Co-treatment with LPS partially reversed these effects.
conclusion1,25(OH)₂D₃ is associated with the attenuation of hyperoxia-induced lung injury and modulation of the TXNIP-NLRP3-GSDMD inflammatory signaling pathway in BPD.
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