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2017 ; 15
(4
): 1702-1712
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Baicalin ameliorates renal fibrosis via inhibition of transforming growth factor
?1 production and downstream signal transduction
#MMPMID28260014
Zheng L
; Zhang C
; Li L
; Hu C
; Hu M
; Sidikejiang N
; Wang X
; Lin M
; Rong R
Mol Med Rep
2017[Apr]; 15
(4
): 1702-1712
PMID28260014
show ga
Previous studies have demonstrated the potential antifibrotic effects of baicalin
in vitro, via examination of 21 compounds isolated from plants. However, its
biological activity and underlying mechanisms of action in vivo remain to be
elucidated. The present study aimed to evaluate the effect of baicalin on renal
fibrosis in vivo, and the potential signaling pathways involved. A unilateral
ureteral obstruction (UUO)?induced renal fibrosis model was established using
Sprague?Dawley rats. Baicalin was administrated intraperitoneally every 2 days
for 10 days. The degree of renal damage and fibrosis was investigated by
histological assessment, and detection of fibronectin and collagen I mRNA
expression levels. Epithelial?mesenchymal transition (EMT) markers, transforming
growth factor-?1 (TGF-?1) levels and downstream phosphorylation of mothers
against decapentaplegic 2/3 (Smad2/3) were examined in vivo and in an NRK?52E rat
renal tubular cell line in vitro. Baicalin was demonstrated to markedly
ameliorate renal fibrosis and suppress EMT, as evidenced by reduced interstitial
collagen accumulation, decreased fibronectin and collagen I mRNA expression
levels, upregulation of N? and E?cadherin expression levels, and downregulation
of ??smooth muscle actin and vimentin expression. Furthermore, baicalin decreased
TGF??1 expression levels in serum and kidney tissue following UUO, and suppressed
Smad2/3 phosphorylation in rat kidney tissue. In vitro studies identified that
baicalin may inhibit the phosphorylation of Smad2/3 under the same TGF??1
concentration. In conclusion, baicalin may protect against renal fibrosis,
potentially via inhibition of TGF??1 production and its downstream signal
transduction.