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Soy isoflavone delays the progression of thioacetamide-induced liver fibrosis in rats

Li, Jian-Fang; Chen, Bi-Cheng; Lai, Dan-Dan; Jia, Zeng-Rong; Andersson, Roland LU ; Zhang, Bo; Yao, Jian-Gao and Yu, Zhen (2011) In Scandinavian Journal of Gastroenterology 46(3). p.341-349
Abstract
Objective. Our aim was to investigate the effect of soy isoflavone (SI) on liver fibrosis in a thioacetamide (TAA)-induced rat model. Materials and methods. Twenty-eight rats were assigned to four groups: sham group, fibrosis group, low-dose treatment group (LDg) and high-dose treatment group (HDg). SI (90 or 270 mg/kg) was administered daily during the model development by TAA. Standard liver tests, platelet derived growth factor-BB (PDGF-BB) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were measured. The expression of collagen, alpha alpha-smooth muscle actin (alpha alpha-SMA) and transforming growth factor-beta beta 1 (TGF-beta beta 1) in liver tissue was determined. Electron microscopy was used to perform ultrastructural... (More)
Objective. Our aim was to investigate the effect of soy isoflavone (SI) on liver fibrosis in a thioacetamide (TAA)-induced rat model. Materials and methods. Twenty-eight rats were assigned to four groups: sham group, fibrosis group, low-dose treatment group (LDg) and high-dose treatment group (HDg). SI (90 or 270 mg/kg) was administered daily during the model development by TAA. Standard liver tests, platelet derived growth factor-BB (PDGF-BB) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were measured. The expression of collagen, alpha alpha-smooth muscle actin (alpha alpha-SMA) and transforming growth factor-beta beta 1 (TGF-beta beta 1) in liver tissue was determined. Electron microscopy was used to perform ultrastructural analysis of the livers. Results. Hepatic fibrosis was induced by 8 weeks of TAA administration. However, following the administration of SI, collagen staining significantly declined as compared with the fibrosis group (p < 0.01). Less collagen fibers around the hepatic stellate cells (HSCs) were observed in HDg as compared to the fibrosis group and LDg. There was no significant difference in standard liver tests between the fibrosis group and the two treatment groups. The levels of PDGF-BB and TIMP-1 in the two SI-treated groups were significantly lower than in the fibrosis group (p < 0.01). The expression of alpha alpha-SMA and TGF-beta beta 1 in HDg was less than that in the fibrosis group and LDg (p < 0.01). Conclusion. Administration of a high dose of SI resulted in an obvious inhibitory effect on liver fibrosis induced by TAA in rats. One hypothesis is that the effect may be related to the inhibition of HSC activation and proliferation. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Isoflavone, liver fibrosis, thioacetamide, rats
in
Scandinavian Journal of Gastroenterology
volume
46
issue
3
pages
341 - 349
publisher
Taylor & Francis
external identifiers
  • wos:000287039100014
  • scopus:79751504859
ISSN
1502-7708
DOI
10.3109/00365521.2010.525662
language
English
LU publication?
yes
id
1c43c354-c077-4aa4-add7-eb28e6718e81 (old id 1878247)
date added to LUP
2011-04-01 08:36:53
date last changed
2017-09-03 04:08:19
@article{1c43c354-c077-4aa4-add7-eb28e6718e81,
  abstract     = {Objective. Our aim was to investigate the effect of soy isoflavone (SI) on liver fibrosis in a thioacetamide (TAA)-induced rat model. Materials and methods. Twenty-eight rats were assigned to four groups: sham group, fibrosis group, low-dose treatment group (LDg) and high-dose treatment group (HDg). SI (90 or 270 mg/kg) was administered daily during the model development by TAA. Standard liver tests, platelet derived growth factor-BB (PDGF-BB) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were measured. The expression of collagen, alpha alpha-smooth muscle actin (alpha alpha-SMA) and transforming growth factor-beta beta 1 (TGF-beta beta 1) in liver tissue was determined. Electron microscopy was used to perform ultrastructural analysis of the livers. Results. Hepatic fibrosis was induced by 8 weeks of TAA administration. However, following the administration of SI, collagen staining significantly declined as compared with the fibrosis group (p &lt; 0.01). Less collagen fibers around the hepatic stellate cells (HSCs) were observed in HDg as compared to the fibrosis group and LDg. There was no significant difference in standard liver tests between the fibrosis group and the two treatment groups. The levels of PDGF-BB and TIMP-1 in the two SI-treated groups were significantly lower than in the fibrosis group (p &lt; 0.01). The expression of alpha alpha-SMA and TGF-beta beta 1 in HDg was less than that in the fibrosis group and LDg (p &lt; 0.01). Conclusion. Administration of a high dose of SI resulted in an obvious inhibitory effect on liver fibrosis induced by TAA in rats. One hypothesis is that the effect may be related to the inhibition of HSC activation and proliferation.},
  author       = {Li, Jian-Fang and Chen, Bi-Cheng and Lai, Dan-Dan and Jia, Zeng-Rong and Andersson, Roland and Zhang, Bo and Yao, Jian-Gao and Yu, Zhen},
  issn         = {1502-7708},
  keyword      = {Isoflavone,liver fibrosis,thioacetamide,rats},
  language     = {eng},
  number       = {3},
  pages        = {341--349},
  publisher    = {Taylor & Francis},
  series       = {Scandinavian Journal of Gastroenterology},
  title        = {Soy isoflavone delays the progression of thioacetamide-induced liver fibrosis in rats},
  url          = {http://dx.doi.org/10.3109/00365521.2010.525662},
  volume       = {46},
  year         = {2011},
}