ArticleFrontiers in pharmacology2025
Anemoside B4 targets RAGE to attenuate ferroptosis in sepsis-induced acute lung injury.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- RAGE Signalling in Acute Inflammatory Disorders: Therapeutic Potential of Natural Products.Biomolecules · 2026Review
- Inhibiting pyruvate carboxylase as a potential therapeutic strategy for alleviating rheumatoid arthritis.Inflammopharmacology · 2026Article
- The RAGE-Ferroptosis Axis Drives Oxidative Stress-Associated Inflammatory Lung Injury in Viral Infection.Antioxidants (Basel, Switzerland) · 2026Article
- Exploring the Effects and Mechanisms of Neohesperidin Dihydrochalcone on Acute Lung Injury in Mice with Sepsis Using Network Pharmacology and Machine Learning.Current issues in molecular biology · 2026Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Natural products in treating sepsis-associated lung and liver injuries by mediating ferroptosis, current progress, and future perspective.Frontiers in pharmacology · 2026Review
- Ferroptosis in sepsis induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS): a potential therapeutic strategy.Frontiers in immunology · 2025Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Anemoside B4 (AB4), a major bioactive saponin isolated from the roots of Methods: To explore the therapeutic mechanism of AB4 in SALI, an integrated approach was employed, combining network pharmacology, molecular dynamics simulation, surface plasmon resonance (SPR) assays, Results: AB4 ameliorated CLP-induced lung injury in mice, as evidenced by reduced pathological damage, lower injury scores, and a decreased lung wet-to-dry weight ratio. Conclusion: AB4 directly targets RAGE to inhibit the AGE/RAGE-Nrf2 axis, thereby suppressing both ferroptosis and inflammation in SALI. This previously unreported mechanism establishes AB4 as a novel multifaceted therapeutic candidate for SALI.
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