Source:http://linkedlifedata.com/resource/pubmed/id/18189272
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2008-5-26
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pubmed:abstractText |
Progressive renal disease is characterized by the accumulation of extracellular matrix proteins in the renal interstitium. Hence, developing agents that antagonize fibrogenic signals is a critical issue facing researchers. The present study investigated the blood-circulation-promoting Chinese herb, safflower, on fibrosis status in NRK-49F cells, a normal rat kidney interstitial fibroblast, to evaluate the underlying signal transduction mechanism of transforming growth factor-beta (TGF-beta), a potent fibrogenic growth factor. Safflower was characterized and extracted using water. Renal fibrosis model was established both in vitro with fibroblast cells treated with beta-hydroxybutyrate and in vivo using rats undergone unilateral ureteral obstruction (UUO). Western blotting was used to examine protein expression in TGF-beta-related signal proteins such as type I and type II TGF-beta receptor, Smads2/3, pSmad2/3, Smads4, and Smads7. ELISA was used to analyze bioactive TGF-beta1 and fibronectin levels in the culture media. Safflower extract (SE) significantly inhibited beta-HB-induced fibrosis in NRK cells concomitantly with dose-dependent inhibition of the type I TGF-beta1 receptor and its down-stream signals (i.e., Smad). Moreover, SE dose-dependently enhanced inhibitory Smad7. Thus, SE can suppress renal cellular fibrosis by inhibiting the TGF-beta autocrine loop. Moreover, remarkably lower levels of tissue collagen were noted in the nephron and serum TGF-beta1 of UUO rats receiving oral SE (0.15 g/3 ml/0.25 kg/day) compared with the untreated controls. Hence, SE is a potential inhibitor of renal fibrosis. We suggest that safflower is a novel renal fibrosis antagonist that functions by down-regulating TGF-beta signals.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Fibronectins,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta1
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1097-4644
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pubmed:author |
pubmed-author:ChangFang-RongFR,
pubmed-author:ChangShan-YuSY,
pubmed-author:ChangWen-TengWT,
pubmed-author:ChiangTai-AnTA,
pubmed-author:ChuangLea-YeaLY,
pubmed-author:GuhJinn-YuhJY,
pubmed-author:HuangJau-ShyangJS,
pubmed-author:HungChien-YaCY,
pubmed-author:HungMin-YuanMY,
pubmed-author:HungTsung-JenTJ,
pubmed-author:LeeTao-ChenTC,
pubmed-author:LiaoTung-NanTN,
pubmed-author:LiuYi-ShiuanYS,
pubmed-author:TengHsiang-ChunHC,
pubmed-author:WangChing-JenCJ,
pubmed-author:YangYu-LinYL,
pubmed-author:YehJeng-HsienJH
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
104
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
908-19
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pubmed:meshHeading |
pubmed-meshheading:18189272-Administration, Oral,
pubmed-meshheading:18189272-Animals,
pubmed-meshheading:18189272-Dose-Response Relationship, Drug,
pubmed-meshheading:18189272-Fibronectins,
pubmed-meshheading:18189272-Fibrosis,
pubmed-meshheading:18189272-Intercellular Signaling Peptides and Proteins,
pubmed-meshheading:18189272-Kidney,
pubmed-meshheading:18189272-Male,
pubmed-meshheading:18189272-Medicine, Chinese Traditional,
pubmed-meshheading:18189272-Models, Biological,
pubmed-meshheading:18189272-Rats,
pubmed-meshheading:18189272-Rats, Sprague-Dawley,
pubmed-meshheading:18189272-Signal Transduction,
pubmed-meshheading:18189272-Transforming Growth Factor beta,
pubmed-meshheading:18189272-Transforming Growth Factor beta1
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pubmed:year |
2008
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pubmed:articleTitle |
Safflower extract: a novel renal fibrosis antagonist that functions by suppressing autocrine TGF-beta.
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pubmed:affiliation |
Department of Biological Science and Technology, Chung Hwa University of Medical Technology, Tainan, Taiwan. call0955443221@gmail.com
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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