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Oxymatrine inhibits collagen synthesis in keloid fibroblasts via inhibition of transforming growth factor‐β1/Smad signaling pathway
Author(s) -
Fan DongLiang,
Zhao WeiJin,
Wang YuXin,
Han SiYuan,
Guo Shu
Publication year - 2012
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1111/j.1365-4632.2011.05234.x
Subject(s) - keloid , oxymatrine , smad , medicine , transforming growth factor , signal transduction , cancer research , western blot , wound healing , fibrosis , blot , microbiology and biotechnology , pharmacology , pathology , immunology , biology , biochemistry , gene
Background Keloids are benign dermal tumors characterized by fibroblastic proliferation and excessive accumulation of collagen. Oxymatrine (OMT) is an alkaloid extracted from the Chinese herb Sophora japonica with capacities of anti‐fibrosis. Objective To evaluate the effects of OMT on collagen production and to explore its mechanisms. Methods OMT was applied to human keloid fibroblasts in vitro . Collagen, transforming growth factor (TGF)‐β1, TGF‐β receptor, and Smads were analyzed by Western Blot, reverse transcription polymerase chain reaction, and immunofluorescence. Results We found that both collagen synthesis and Smad3 production were significantly suppressed in a dose‐dependent administration of OMT. However, expression of TGF‐β1, TGF‐β receptor1, TGF‐β receptor2, Smad4, and Smad7 was unchanged. We also found that OMT reversed phosphorylation and nuclear translocation of Smad3 induced by TGF‐β1. Conclusions OMT inhibited collagen synthesis, which might be associated with TGF‐β/Smad signaling pathway. These findings suggest that OMT may be a promising candidate to prevent keloid and other fibrotic diseases.