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2016 ; 11
(3
): 998-1004
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gab.com Text
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Curcumin suppresses transforming growth factor-?1-induced cardiac fibroblast
differentiation via inhibition of Smad-2 and p38 MAPK signaling pathways
#MMPMID26998027
Liu H
; Liu A
; Shi C
; Li B
Exp Ther Med
2016[Mar]; 11
(3
): 998-1004
PMID26998027
show ga
The differentiation of cardiac fibroblasts (CFs) into myofibroblasts and the
subsequent deposition of the extracellular matrix is associated with myocardial
fibrosis following various types of myocardial injury. In the present study, the
effect of curcumin, which is a pharmacologically-safe natural compound from the
Curcuma longa herb, on transforming growth factor (TGF)-?1-induced CFs was
investigated, and the underlying molecular mechanisms were examined. The
expression levels of ?-smooth muscle actin (SMA) stress fibers were investigated
using western blotting and immunofluorescence in cultured neonatal rat CFs.
Protein and mRNA expression levels of ?-SMA and collagen type I (ColI) were
determined by western blotting and reverse transcription-quantitative polymerase
chain reaction. In addition, the activation of Smad2 and p38 was examined using
western blotting. Curcumin, SB431542 (a TGF-?R-Smad2 inhibitor) and SB203580 (a
p38 inhibitor) were used to inhibit the stimulation by TGF-?1. The results
demonstrated that the TGF-?1-induced expression of ?-SMA and ColI was suppressed
by curcumin at the mRNA and protein levels, while SB431542 and SB203580 induced
similar effects. Furthermore, phosphorylated Smad-2 and p38 were upregulated in
TGF-?1-induced CFs, and these effects were substantially inhibited by curcumin
administration. In conclusion, the results of the present study demonstrated that
treatment with curcumin effectively suppresses TGF-?1-induced CF differentiation
via Smad-2 and p38 signaling pathways. Thus, curcumin may be a potential
therapeutic agent for the treatment of cardiac fibrosis.