ArticleFrontiers in pharmacology2025
Galangin ameliorates PTU-induced vitiligo in zebrafish and B16F10 cells by increasing melanogenesis through activation of the p38/JNK MAPK 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 6 papers.
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6 citing papers in PubMed.
- Pharmacological Mechanisms of Active Constituents from Traditional Chinese Medicine for Vitiligo Treatment.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Combining bioinformatics prediction with experimental validation to explore the ameliorative effect ofMolecular medicine reports · 2026Article
- Role of MAPK Pathways in the Pathogenesis of Vitiligo.Current issues in molecular biology · 2026Review
- Evaluation of the antioxidant and anti-inflammatory efficacy of fermentedBiochemistry and biophysics reports · 2026Article
- recent advances in the pathogenesis of vitiligo and the application of novel drug delivery systems in its treatment.International journal of pharmaceutics: X · 2025Review
- Repurposing the Antibiotic D-Cycloserine for the Treatment of Hyperpigmentation: Therapeutic Potential and Mechanistic Insights.International journal of molecular sciences · 2025Article
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Abstract
Objective: Methods: In this study, 1-phenyl-2-thiourea (PTU) was used to establish a vitiligo model in zebrafish. After successful modeling, different concentrations of GA (1 and 2 μM) were administered, and the distribution of melanin granules was observed by assaying the melanin content, masson-fontana staining and tyrosinase activity. Transcriptomic analysis and molecular docking were used to identify potential GA-related pathways and targets for improving vitiligo. In addition, we evaluated the proliferation of B16F10 cells by PTU induction and also observed cellular melanin distribution using masson-fontana staining. Finally, Western blot was performed to detect the proteins of the relevant pathways. Results: The results showed that GA significantly increased melanin production and tyrosinase activity in depigmented zebrafish. In addition, we found that GA decreased ROS and MDA levels and increased the expression of GSH, CAT and T-SOD. In addition, transcriptome analysis indicated that GA likely acts through the mitogen-activated protein kinase (MAPK) signaling pathway. GA has a strong binding affinity for important targets.GA significantly increased the expression of genes such as mapk8b, mapk14a, mapk3, mitf, tyr, tyrp1b, tyrp1a, dct, and oca2, and decreased the expression of genes such as expression of genes such as raf1 and egfr. In addition, GA enhanced the viability of B16F10 cells, increased intracellular melanin content, and increased the expression of proteins such as p38, JNK1/2/3, TYR, MITF, TRP1, TRP2, and so on. Conclusion: GA increases melanin production and distribution, improves tyrosinase activity, upregulates the expression of related genes and proteins through activation of MAPK and tyrosine metabolic pathways, downregulates oxidative stress, and then regulates changes in melanin synthesis to improve vitiligo.
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