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PRECLINICAL PUBLICATION · 2019

Insulin ameliorates pulmonary edema through the upregulation of epithelial sodium channel via the PI3K/SGK1 pathway in mice with lipopolysaccharide-induced lung injury.

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 30628684 ↗2019Reported benefit

Insulin ameliorates pulmonary edema through the upregulation of epithelial sodium channel via the PI3K/SGK1 pathway in mice with lipopolysaccharide-induced lung injury.

MouseEndotoxin/LPSC3H/HeNn = 24 mice in four groups, n=6 per groupIntravenous via an internal jugular vein catheter attached to a micro-osmotic pump0.1 U/kg/h at a rate of 2.5 mU/h per mouseStarted 16 h prior to lipopolysaccharide exposure

Model: Lipopolysaccharide-induced acute lung injury, LPS serotype O111:B4 at 5 mg/kg in 50 ul by one-time intratracheal injection, without hyperglycaemia

Insulin reduced lavage protein, cell and neutrophil counts, epithelial permeability, lung injury score, wet to dry ratio and apoptosis and increased alveolar fluid clearance by 93% through increased ENaC expression and SGK1 phosphorylation, without altering blood glucose.

Extraction: extract · Supplied extraction confidence: 0.85. Machine-extracted fields require source verification.