Abstract:
:To investigate mechanisms of protective effects of fenofibrate on the diabetic kidney, male Wistar rats were divided into control, untreated diabetes, and fenofibrate-treated (32 mg kg(-1) d(-1), 8 weeks) diabetes groups. Diabetes induced by streptozotocin (25 mg/kg) and a high-fat diet was characterized by the disorders of plasma glucose and lipids. In untreated diabetic rats, there were increases in glomerular volume, matrix content, expressions of laminin and urinary albumin excretion. These nephropathies were associated with the upregulations of plasminogen activator inhibitor 1 (PAI-1) mRNA expression and its protein activity in the renal cortex, and a significant increase in transforming growth factor beta1 (TGF-beta1) expression. Treatment with fenofibrate suppressed the expression of PAI-I mRNA and its protein activity, and inhibited TGF-beta1 overexpression. It also partially reversed metabolic disorders and pathophysiologic changes associated with diabetic nephropathy. Our results indicate that fenofibrate delays the progression of diabetic nephropathy in rats to some extent. These renoprotective effects are likely to be achieved through suppression of PAI-1 and TGF-beta1 in the renal cortex, and consequently less extracellular matrix deposition.
journal_name
Vascul Pharmacoljournal_title
Vascular pharmacologyauthors
Chen LL,Zhang JY,Wang BPdoi
10.1016/j.vph.2006.01.004subject
Has Abstractpub_date
2006-05-01 00:00:00pages
309-15issue
5eissn
1537-1891issn
1879-3649pii
S1537-1891(06)00023-1journal_volume
44pub_type
杂志文章abstract::Bemiparin is a low molecular weight heparin (LMWH) indicated for the acute treatment of deep vein thrombosis with or without pulmonary embolism, for the prophylaxis of venous thromboembolism in surgical and non-surgical patients and for the prevention of clotting in the extracorporeal circuit during hemodialysis. Due ...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
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journal_title:Vascular pharmacology
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journal_title:Vascular pharmacology
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doi:10.1016/j.vph.2006.10.002
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journal_title:Vascular pharmacology
pub_type: 杂志文章
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2006.01.002
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2003.09.002
更新日期:2003-12-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2015.10.006
更新日期:2016-04-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.08.007
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2008.11.005
更新日期:2009-03-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2019.106577
更新日期:2019-10-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2006.05.006
更新日期:2006-12-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2010.07.003
更新日期:2010-09-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2014.04.003
更新日期:2014-05-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2017.03.005
更新日期:2017-05-01 00:00:00
abstract::Increasing evidences support that PGC-1α participates in regulating endothelial homeostasis, in part by mediating endothelial nitric oxide (NO) synthase (eNOS) activity and NO production. However, the molecular mechanisms by which PGC-1α regulates eNOS activity are not completely understood. In the present study, we i...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.05.005
更新日期:2016-08-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2018.07.001
更新日期:2018-11-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2012.02.003
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
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journal_title:Vascular pharmacology
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doi:10.1016/j.vph.2013.12.003
更新日期:2014-02-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2019.106613
更新日期:2020-01-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.08.008
更新日期:2016-12-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2005.10.003
更新日期:2006-02-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2012.01.008
更新日期:2012-03-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2015.02.001
更新日期:2015-04-01 00:00:00
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journal_title:Vascular pharmacology
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/s1537-1891(03)00042-9
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abstract::We investigated the regulation of the epithelial sodium channel (ENaC) in human bone marrow endothelial cells (HBMEC) responding to mineralocorticoid hormones and other accessory effectors. The message for both the mineralocorticoid receptor (MCR) and the alpha subunit of ENaC was expressed in HBMEC as predicted bands...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2003.08.003
更新日期:2004-01-01 00:00:00
abstract::Atherosclerosis is a complex multifactorial disease that affects large and medium-sized arteries. Rupture of atherosclerotic plaques and subsequent acute cardiovascular complications remain a leading cause of death and morbidity in the Western world. There is a considerable difference in safety profile between a stabl...
journal_title:Vascular pharmacology
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doi:10.1016/j.vph.2018.06.014
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