Abstract：
BACKGROUND:Processes of restenosis, following arterial injury, are complex involving different cell types producing various cytokines and enzymes. Among those enzymes, smooth muscle cell-derived matrix metalloproteinases (MMPs) are thought to take part in cell migration, degrading of extracellular matrix, and neointima formation. MMP-9, also known as gelatinase B, is expressed immediately after vascular injury and its expression and activity can be inhibited by statins. Using an established in vivo model of vascular injury, we investigated the effect of the HMG-CoA reductase inhibitor rosuvastatin on MMP-9 expression and neointima formation. MATERIALS AND METHODS:14-week old male Sprague Dawley rats underwent balloon injury of the common carotid artery. Half of the animals received rosuvastatin (20 mg/kg body weight/day) via oral gavage, beginning 3 days prior to injury. Gelatinase activity and neointima formation were analyzed 3 days and 14 days after balloon injury, respectively. 14 days after vascular injury, proliferative activity was assessed by staining for Ki67. RESULTS:After 14 days, animals in the rosuvastatin group showed a decrease in total neointima formation (0.194±0.01 mm2 versus 0.124±0.02 mm2, p<0.05) as well as a reduced intima/media ratio (1.26±0.1 versus 0.75±0.09, p<0.05). Balloon injury resulted in increased activity of MMP-9 3 days after intervention for both rosuvastatin treated animals and controls with no significant difference observed between the groups. There was a trend towards a reduction in the number of Ki67-positive cells 14 days after injury. CONCLUSIONS:Rosuvastatin attenuates neointima formation without affecting early MMP-9 activity in a rat model of vascular injury.
journal_name
Eur J Med Resjournal_title
European journal of medical researchauthors
Preusch MR,Vanakaris A,Bea F,Ieronimakis N,Shimizu T,Konstandin M,Morris-Rosenfeld S,Albrecht C,Kranzhöfer A,Katus HA,Blessing E,Kranzhöfer Rdoi
10.1186/2047-783x-15-11-461subject
Has Abstractpub_date
2010-11-25 00:00:00pages
461-7issue
11eissn
0949-2321issn
2047-783Xjournal_volume
15pub_type
杂志文章abstract：INTRODUCTION:Mitochondrial dysfunction plays a central role in the general pathogenesis of non-alcoholic fatty liver disease (NAFLD), increasing the risk of developing steatosis and subsequent hepatocellular inflammation. We aimed to assess hepatic mitochondrial function by a non-invasive (13)C-methionine breath test (...
journal_title：European journal of medical research
pub_type： 杂志文章
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journal_title：European journal of medical research
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journal_title：European journal of medical research
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journal_title：European journal of medical research
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journal_title：European journal of medical research
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journal_title：European journal of medical research
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journal_title：European journal of medical research
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journal_title：European journal of medical research
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journal_title：European journal of medical research
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