ArticleHistology and histopathology2025
Luteoloside ameliorates sepsis-induced acute lung injury via AMPK-ULK1 pathway-mediated autophagy.
Article in Histology and histopathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Epigallocatechin-3-gallate ameliorates lipopolysaccharide-induced inflammation via the 67LR/JAK2/STAT3 signaling pathway.Scientific reports · 2025Article
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6 authors.
Funding
Abstract
backgroundSeptic patients are at high risk of acute lung injury (ALI). Luteoloside is a flavonoid isolated from natural herbs and has many beneficial effects. This study aimed to investigate the protective role of luteoloside in sepsis-induced ALI.
methodsSepsis was induced by cecal ligation and puncture (CLP) in C57BL/6 mice. Inflammation was induced by lipopolysaccharide (LPS) in MLE-12 cells. The survival rate over 12 days, histological changes in lung and heart, pulmonary edema, vascular leakage, hypoxemia, and inflammation were examined. Apoptosis was detected by TUNEL staining
resultsLuteoloside attenuated lung and cardiac injury, pulmonary edema, vascular leakage, hypoxemia, and inflammation and improved the survival of septic mice. Luteoloside (20 mg/kg) had no toxic effect on the heart, liver, spleen, and kidney in normal mice. Luteoloside enhanced autophagy to inhibit apoptosis
conclusionOverall, luteoloside activates AMPK/ULK1 signaling to stimulate autophagy, thereby inhibiting apoptosis and alleviating sepsis-induced ALI.
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