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Effect of captopril on collagen metabolisms in keloid fibroblast cells
Author(s) -
Chen Junjie,
Zhao Sha,
Liu Yong,
Cen Ying,
Nicolas Crook
Publication year - 2016
Publication title -
anz journal of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.426
H-Index - 70
eISSN - 1445-2197
pISSN - 1445-1433
DOI - 10.1111/ans.12670
Subject(s) - keloid , captopril , fibroblast , medicine , cancer research , platelet derived growth factor receptor , transforming growth factor , wound healing , growth factor , pharmacology , endocrinology , pathology , biochemistry , immunology , biology , in vitro , receptor , blood pressure
Background Keloid is a proliferative disease of fibrous tissues. The mechanism and consistently effective treatments of keloid remained unknown. Although there was a report about treating keloid with topical captopril, the further investigation about captopril affecting keloid has not been performed so far. Objectives The aim of this study was to analyse the effect of captopril on collagen metabolisms in keloid fibroblast cells, and to provide information for the mechanism and therapy of keloid. Methods To investigate the effects and relative mechanism of captopril on keloid fibroblast cells, we examined the changes of collagen metabolism, expression of angiotensin, transforming growth factor ( TGF )‐β1, platelet‐derived growth factor (PDGF ) ‐BB and heat shock protein 47 ( HSP 47), and cellular proliferation in keloid fibroblast cells. Results We found that all collagen metabolisms, expression of TGF ‐β1, PDGF‐BB and HSP 47, and cellular proliferation decreased significantly with effective captopril concentrations in keloid fibroblast cells. Conclusions With a comprehensive analysis of test results, we proposed that captopril may decrease the expression of angiotensin, PDGF‐BB , TGF ‐β1 and HSP 47, and further inhibit proliferation and collagen synthesis of keloid fibroblast cells, which were the key in keloid formation.