Abstract
Background Hypertrophic scar (HS) is a benign fibroproliferative skin disease resulting from an aberrant wound healing process and can cause aesthetic and functional damage to patients. Currently, there is no ideal treatment to treat this disease. Galangin, a natural active bioflavonoid compound, is suggested to inhibit fibrosis and proliferation in certain cells. Methods In this study, we found Galangin could attenuate abnormal scar formation in an HS rabbit ear model. Additionally, the HE staining shows Galangin reduced scar elevation index (SEI) and Masson's trichrome staining changed collagen deposition. Results The expressions of type I collagen, type III collagen, and TGF-β1 were much lower under a proper dose of Galangin treatment, and Smad7 expression was also enhanced, which are examined by real-time PCR, immunohistochemistry, and western blot. Conclusion Our data indicated that Galangin can alleviate dermal scarring via the TGF-β/Smad signaling pathway probably by upregulating Smad 7 expression and, thus, suppressing the expression of type I and type III collagens and TGF-β1.
Highlights
Hypertrophic scar (HS) is a benign fibroproliferative skin disease resulting from an aberrant wound healing process and can cause aesthetic and functional damage to patients
To dynamically observe the scar-forming progress and the effect of Galangin on scar formation since day 15 after wounding (Figure 1(a)), the scars were observed every day and photographed before each injection. e intralesional Galangin injection groups showed obvious softness after the second injection compared with the control group (Figure 1(b))
Bioflavonoid has been proved to alleviate fibrosis in the liver [15]. us, based on the abovementioned study, we assumed that Galangin could suppress HS formation, and this assumption is proved in our further investigation which shows that Galangin could soften the HSs and decrease the scar elevation index (SEI) of the rabbit ear model in vivo
Summary
Hypertrophic scar (HS) is a benign fibroproliferative skin disease resulting from an aberrant wound healing process and can cause aesthetic and functional damage to patients. Our data indicated that Galangin can alleviate dermal scarring via the TGF-β/Smad signaling pathway probably by upregulating Smad 7 expression and, suppressing the expression of type I and type III collagens and TGF-β1. Scarring is an inevitable natural process during wound healing. E wound healing progress is a complex one which involves many types of cells, mediators, and three sequential steps: inflammation, new tissue formation, and remodeling [1, 2]. Collagen is overdeposited in the extracellular matrix (ECM), and the fibroblasts become overproliferated during the remodeling phase of wound healing [5]. Wound healing ends up with HS formation, which may cause dysfunction, pain, aesthetic problem, etc. Several decades have been spent to searching optimal treatments for HS, it remains an unmet challenge
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