Korean J Dermatol.
2012 Jan;50(1):1-7.
Curcumin Induced Decreased Expression of Type I Collagen in Human Skin Fibroblast Through Down-regulation of Smad2/3 Expressions
- Affiliations
-
- 1Department of Dermatology, School of Medicine, Keimyung University, Daegu, Korea. janylove99@dsmc.or.kr
- 2Department of Pathology, School of Medicine, Keimyung University, Daegu, Korea.
Abstract
- BACKGROUND
Imbalance among TGF-beta/Smad pathway, MMP-1, and TIMP-1 expressions results in sclerotic skin disease, such as scleroderma, hypertrophic scar, and keloids. Curcumin, a phytochemical extracted from the rhizomes of Curcuma longa, showed an anti-fibrotic effect in an animal study, such as a pulmonary and cholangioductal fibrosis animal model. However, the expressions of type I collagen, MMP-1, Smad2/3, and TIMP-1 in curcumin treated human skin fibroblasts is largely unknown.
OBJECTIVE
The purpose of this study was to investigate the expressions of type I collagen, MMP-1, Smad2/3, and TIMP-1 proteins in curcumin-treated human skin fibroblasts.
METHODS
Human skin fibroblasts were treated by various concentrations of curcumin (1~40 uM). The expressions of type I collagen, MMP-1, Smad2/3, and TIMP-1 proteins were analyzed by Western blot analysis. In addition, activities of type I collagen promoter were analyzed by the CAT assay.
RESULTS
The expression of type I collagen decreased but the expression of MMP-1 and TIMP-1 increased by curcumin treatment in a dose and time dependent manner in Western blot analysis. Type I collagen promoter activities were decreased by curcumin treatment in the CAT assay. Smad2/3 expression decreased by curcumin treatment but TGF-beta1 induced Smad2/3 activation was not decreased by curcumin treatment following Western blot analysis.
CONCLUSION
Decrease of type I collagen expression through the inhibition of Smad2/3 and increase of the expression of MMP-1, which is the degradating enzyme of type I collagen, in human skin fibroblasts by curcumin treatment offer expectation of curcumin as antifibrotic agent.