ArticleExperimental biology and medicine (Maywood, N.J.)2024
Berberine alleviates AGEs-induced ferroptosis by activating NRF2 in the skin of diabetic mice.
Article in Experimental biology and medicine (Maywood, N.J.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- The Role of Ferroptosis in Diabetes Pathogenesis: Therapeutic Implications of Hydrogen Sulfide and Its Reactive Metabolites.Antioxidants (Basel, Switzerland) · 2026Review
- Dietary advanced glycation products combined with chronic restraint stress induced anxiety-like and depression-like behaviors in male mice.NPJ science of food · 2026Article
- Berberine-induced ferroptosis as a novel anti-cancer strategy: Molecular, epigenetic and translational perspectives.EXCLI journal · 2026Review
- Research progress on the role and mechanisms of ferroptosis in diabetic wound repair.Cell death discovery · 2025Review
- Ferroptosis in diabetes mellitus and its complications: overview of clinical and preclinical research.Cell death discovery · 2025Review
- Potential of Natural Products in Hangeshashinto Water Extract on the Direct Suppression of Stomatitis Induced by Intra-/Extracellular Advanced Glycation End-Products.International journal of molecular sciences · 2025Review
- Phytochemicals as modulators of ferroptosis: a novel therapeutic avenue in cancer and neurodegeneration.Molecular biology reports · 2025Review
- Integrating clinical evidence with natural product therapies for elderly-onset type 2 diabetes.Frontiers in pharmacology · 2025Review
- Mechanistic Perspectives on Radiation-Induced Skin Injury and the Protective Effects of Berberine.Journal of inflammation research · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
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Abstract
Advanced glycation end products (AGEs) have adverse effects on the development of diabetic complications. Berberine (BBR), a natural alkaloid, has demonstrated its ability to promote the delayed healing of skin wounds. However, the impact of BBR on AGEs-induced ferroptosis in skin cells and the underlying molecular mechanisms remains unexplored. This study investigated the involvement of ferroptosis in AGEs-induced keratinocyte death, and the impact of BBR on ferroptosis in a db/db mouse model with long-term hyperglycemia was elucidated. A remarkable reduction in cell viability was observed along with increased malondialdehyde (MDA) production in AGEs-induced HaCaT cells. Intracellular reactive oxygen species (ROS) and iron levels were elevated in cells exposed to AGEs. Meanwhile, the protein expression of glutathione peroxidase 4 (GPX4) and ferritin light chain (FTL) was significantly decreased in AGEs-treated cells. However, pretreatment with BBR markedly protected cell viability and inhibited MDA levels, attenuating the intracellular ROS and iron levels and increased expression of GPX4 and FTL
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