ArticleInflammopharmacology2025
Kirenol ameliorates endotoxin-induced acute lung injury by inhibiting the ERK and JNK phosphorylation-mediated NFκB pathway in mice.
Article in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Visnagin Protects Against Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting Oxidative Stress and Reducing Ferroptosis.International journal of medical sciences · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
Acute lung injury (ALI) is a pathological condition characterised by varying degrees of lung damage in patients. Kirenol exerts anti-inflammatory, immunosuppressive, and antioxidative effects. We investigated the protective effects of kirenol on lipopolysaccharide-induced ALI in mice. Pretreatment with kirenol significantly ameliorated lung oedema and neutrophil infiltration in ALI mice. Kirenol downregulated the chemokines (MIP-2) expression and the adhesion molecules (ICAM-1 and VCAM-1) secretion. Furthermore, kirenol inhibited the production of the proinflammatory mediators nitric oxide and prostaglandin (PG)E2 through the upstream factors iNOS and cyclooxygenase (COX)-2, respectively. Kirenol suppressed the IKK-IκB-NFκB pathway, which is involved in lipopolysaccharide-induced inflammation. Kirenol inhibited the lipopolysaccharide-induced phosphorylation of ERK and JNK, to a lesser extent, p38 MAPK and Akt. In conclusion, our findings suggest that kirenol exerts ameliorative effects against ALI by suppressing the production of chemokines, adhesion molecules, and proinflammatory mediators and inhibiting the IKK-IκB-NFκB pathway and its upstream factors, phosphorylated ERK and JNK.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.