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PRECLINICAL PUBLICATION · 2020

Vitamin D attenuates lung injury via stimulating epithelial repair, reducing epithelial cell apoptosis and inhibits TGF-beta induced epithelial to mesenchymal transition.

Mouse / Endotoxin/LPS

Evidence by therapy association

Study details and outcomes are extracted in the context of a specific intervention. Separate associations are retained rather than silently merged.

PMID 32251673 ↗2020Reported benefit

Vitamin D attenuates lung injury via stimulating epithelial repair, reducing epithelial cell apoptosis and inhibits TGF-beta induced epithelial to mesenchymal transition.

MouseEndotoxin/LPSC57BL/6Male and femaleIntragastric0.1, 1.5 and 10 mg/kgPretreatment for 14 days before intratracheal lipopolysaccharide

Model: Intratracheal lipopolysaccharide-induced acute lung injury in mildly vitamin D deficient mice; supported by primary human and murine type II alveolar epithelial cell work

Vitamin D supplementation promoted alveolar type II cell proliferation, inhibited apoptosis and inhibited epithelial to mesenchymal transition, attenuating lipopolysaccharide-induced lung injury; in vitro it stimulated epithelial scratch wound repair through vitamin D receptor dependent PI3K/Akt si…

Extraction: extract · Supplied extraction confidence: 0.7. Machine-extracted fields require source verification.