ArticleFrontiers in pharmacology2025
Berberine protects against gefitinib-induced liver injury by inhibiting the HMGB1/TLR4/NF-κB pathway.
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 2 papers.
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2 citing papers in PubMed.
- Integrating polyphenols and exercise in cancer prevention, treatment, and rehabilitation: cellular and molecular mechanisms linking the injury-recovery-musculoskeletal resilience axis.Frontiers in oncology · 2026Review
- Natural compounds for non-small cell lung cancer treatment: focus on the EGFR signaling pathway.Frontiers in pharmacology · 2026Review
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6 authors.
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Abstract
Background: Gefitinib (GEF), a first-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) for non-small cell lung cancer (NSCLC), is frequently associated with drug-induced liver injury (DILI), thereby limiting its clinical application. This study aimed to evaluate the hepatoprotective effects of berberine (BBR) and explore the underlying mechanisms. Methods: Results: GEF activated the HMGB1/TLR4/NF-κB pathway Conclusion: GEF-induced liver injury is mediated by HMGB1-driven inflammation via the TLR4/NF-κB pathway. BBR provides dose-dependent hepatoprotection by targeting this pathway, suggesting a potential strategy to protect against GEF-induced liver injury among NSCLC patients.
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