The use of low molecular weight heparin-pluronic nanogels to impede liver fibrosis by inhibition the TGF-β/Smad signaling pathway

Title
The use of low molecular weight heparin-pluronic nanogels to impede liver fibrosis by inhibition the TGF-β/Smad signaling pathway
Authors
이주희이현승정윤기정경희최종훈이돈행박기동홍순선
Keywords
low molecular weight heparin; heparin-pluronic nanogel; DMN; liver fibrosis; TGF-β/Smad; anti-fibrotic agent
Issue Date
2011-02
Publisher
Biomaterials
Citation
VOL 32, NO 5, 1438-1445
Abstract
Low molecular weight heparin (LH) has been reported to have anti-fibrotic and anti-cancer effects. To enhance the efficacy and minimize adverse effects of LH, a low molecular weight heparinepluronic nanogel (LHP) was synthesized by conjugating carboxylated pluronic F127 to LH. The LHP reduced anticoagulant activity by about 33% of the innate activity. Liver fibrosis was induced by the injection of 1% dimethylnitrosamine (DMN) in rats, and LH or LHP (1000 IU/kg body weight) was treated once daily for 4 weeks. LHP administration prevented DMN-mediated liver weight loss and decreased the values of aspartate transaminase, alanine transaminase, total bilirubin, and direct bilirubin. LHP markedly reduced the fibrotic area compared to LH. Also, LHP potently inhibited mRNA or protein expression of alphasmooth muscle actin, collagen type I, matrix metalloproteinase-2, and tissue inhibitor of metalloproteinase- 1 compared to LH, in DMN-induced liver fibrosis. In addition, LHP decreased the expression of transforming growth factor-b1 (TGF-b1), p-Smad 2, and p-Smad 3, which are all important molecules of the TGF-b/Smad signaling pathway. The results support an LHP shows anti-fibrotic effect in the liver via inhibition of the TGF-b/Smad pathway as well as by the elimination of the extracellular matrix.
URI
http://pubs.kist.re.kr/handle/201004/41359
ISSN
0142-9612
Appears in Collections:
KIST Publication > Article
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE