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Abstract Title:

Galangin inhibits hypertrophic scar formation via ALK5/Smad2/3 signaling pathway.

Abstract Source:

Mol Cell Biochem. 2016 Feb ;413(1-2):109-18. Epub 2016 Jan 4. PMID: 26728998

Abstract Author(s):

Yifan Zhang, Shengzhou Shan, Jing Wang, Xinyu Cheng, Bo Yi, Jia Zhou, Qingfeng Li

Article Affiliation:

Yifan Zhang

Abstract:

Hypertrophic scar (HS) is characterized by excessive fibrosis associated with aberrant function of fibroblasts. Currently, no satisfactory drug has been developed to treat the disease. Here we found that a flavonoid natural product, galangin, could significantly attenuate hypertrophic scar formation in a mechanical load-induced mouse model. Both in vivo and in vitro studies demonstrated that galangin remarkably inhibited collagen production, proliferation, and activation of fibroblasts. Besides, galangin suppressed the contractile ability of hypertrophic scar fibroblasts. Further Western blot analysis revealed that galangin dose-dependently down-regulated Smad2 and Smad3 phosphorylation. Such bioactivity of galangin resulted from its selective targeting to the activin receptor-like kinase 5 (ALK5) was demonstrated by ALK5 knockdown and over-expression experiments. Taken together, this compound could simultaneously inhibit both the accumulation of collagen and abnormal activation/proliferation of fibroblasts, which were the two pivotal factors for hypertrophic scar formation, thus suggesting that galangin serves as a potential agent for treatment of HS or other fibroproliferative disorders.

Study Type : In Vitro Study
Additional Links
Pharmacological Actions : Antiproliferative : CK(6801) : AC(5032)

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