ArticleJournal of molecular histology2025
Chrysin inhibits hypertrophic scar formation through TGF-β/Smad signaling pathways.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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8 authors.
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Abstract
Hypertrophic scar (HS) is a complex fibrotic skin condition characterized primarily by proliferation of abnormal fibroblasts and accumulation of excessive extracellular matrix (ECM). Chrysin (CHR), a naturally occurring flavonoid compound, has been shown to exhibit anti-fibrotic properties in multiple disease models. The aim of this study was to explore the effects of CHR on HS and its underlying mechanisms. TGF-β1-induced HDF-α (Human Dermal Fibroblasts) served as an in vitro model of HS. Following treatment with CHR, cellular viability, proliferation, migration, and contractile capacity were evaluated through CCK-8, EdU, Transwell, wound healing, and collagen gel contraction assays. Western blot analysis was conducted to evaluate the expression levels of PCNA, MMP-2, α-SMA, Collagen I, and Collagen III, along with the activation status of the TGF-β/Smad signaling pathway. In vivo, histological analysis of rabbit ear HS tissues demonstrated that CHR ameliorated fibroblast proliferation and improved collagen fiber organization. Furthermore, immunohistochemical and Western blot analyses showed that CHR downregulated the expression levels of α-SMA, Collagen I, and Collagen III. Therefore, CHR may be a potential drug for the prevention and treatment of HS.
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