ArticleThe Journal of endocrinology2026
Leonurine alleviates lung ischemia-reperfusion injury through suppression of ferroptosis via RORα in male mice.
Article in The Journal of endocrinology, 2026. 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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Who cites it
1 citing paper in PubMed.
- Necroptosis in alveolar epithelium orchestrates lung ischemia-reperfusion injury: a multi-omics study.Respiratory research · 2026Article
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6 authors.
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Abstract
Lung ischemia-reperfusion injury (LIRI) is a complex pathological condition that significantly impairs clinical outcomes following lung transplantation and thoracic surgery. Leonurine (LEO), an alkaloid derived from Leonurus japonicus, which has known anti-inflammatory and antioxidant properties, has shown therapeutic potential in various oxidative stress-related diseases. However, the effects of LEO on LIRI and its underlying mechanisms remain unclear. In the present study, a murine model of LIRI was established using wild-type mice. LEO treatment significantly improved lung histopathology, reduced oxidative stress, decreased pulmonary edema, and enhanced survival. Bioinformatics analyses - including volcano plot, KEGG enrichment, and GSEA - identified ferroptosis as a key regulatory pathway. In vivo and in vitro assays (HE, 4-HNE, and DHE labeling; immunofluorescence; and immunoblotting) confirmed that LEO inhibited ferroptosis in lung tissue and in MLE-12 cells. Mechanistically, LEO upregulated the RORα/Nrf2/GPX4 axis, thereby reducing lipid peroxidation and iron overload, as validated by BODIPY581/591 C11 and FeRhoNox-1 staining. Moreover, RORα inhibition abolished the anti-ferroptotic effects of LEO, indicating that its protective function is RORα dependent. Molecular docking further supported a potential direct interaction between LEO and RORα. Collectively, LEO alleviates LIRI by inhibiting ferroptosis through activation of the RORα/Nrf2/GPX4 signaling pathway. These findings suggest that LEO may serve as a promising therapeutic agent for the treatment of LIRI.
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