Source:http://linkedlifedata.com/resource/pubmed/id/19166837
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2009-3-20
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| pubmed:abstractText |
Simvastatin, a cholesterol-lowering agent, has demonstrated neuroprotective effects against brain injury, but the underlying mechanisms remain unclear. This study was undertaken to evaluate the effect of simvastatin on the Toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-kappaB) related signaling pathway and secondary brain injury in rats after traumatic brain injury (TBI). Adult male Wistar rats were divided into four groups: (1) Sham group (n=25); (2) Sham+vehicle group (n=25); (3) TBI+vehicle group (n=30); and (4) TBI+simvastatin group (n=30). Right parietal cortical contusion was made by using a weight-dropping method. In TBI+simvastatin group, simvastatin was administered orally at a dose of 37.5 mg/kg at 1 and 6 h after TBI. Brain samples were extracted at 24 h after trauma. As a result, we found that treatment with simvastatin markedly inhibited the mRNA and protein expressions of TLR4, NF-kappaB and the downstream inflammatory agents, such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and intercellular adhesion molecule-1 (ICAM-1). Administration of simvastatin following TBI significantly ameliorated the secondary brain damage, such as cortical apoptosis, brain edema, blood-brain barrier (BBB) impairment, and motor deficits. In conclusion, post-TBI simvastatin administration may attenuate TLR4/NF-kappaB-mediated inflammatory response in the injured rat brain, and this may be one mechanism by which simvastatin improves outcome following TBI.
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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/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxymethylglutaryl-CoA...,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Simvastatin,
http://linkedlifedata.com/resource/pubmed/chemical/Tlr4 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 4
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
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| pubmed:issn |
1090-2430
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
216
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
398-406
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| pubmed:meshHeading |
pubmed-meshheading:19166837-Analysis of Variance,
pubmed-meshheading:19166837-Animals,
pubmed-meshheading:19166837-Apoptosis,
pubmed-meshheading:19166837-Blood-Brain Barrier,
pubmed-meshheading:19166837-Brain Edema,
pubmed-meshheading:19166837-Brain Injuries,
pubmed-meshheading:19166837-Cytokines,
pubmed-meshheading:19166837-Disease Models, Animal,
pubmed-meshheading:19166837-Electrophoretic Mobility Shift Assay,
pubmed-meshheading:19166837-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:19166837-Gene Expression Regulation,
pubmed-meshheading:19166837-Hydroxymethylglutaryl-CoA Reductase Inhibitors,
pubmed-meshheading:19166837-In Situ Nick-End Labeling,
pubmed-meshheading:19166837-Intercellular Adhesion Molecule-1,
pubmed-meshheading:19166837-Male,
pubmed-meshheading:19166837-Movement Disorders,
pubmed-meshheading:19166837-NF-kappa B,
pubmed-meshheading:19166837-Rats,
pubmed-meshheading:19166837-Rats, Wistar,
pubmed-meshheading:19166837-Rotarod Performance Test,
pubmed-meshheading:19166837-Signal Transduction,
pubmed-meshheading:19166837-Simvastatin,
pubmed-meshheading:19166837-Time Factors,
pubmed-meshheading:19166837-Toll-Like Receptor 4
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| pubmed:year |
2009
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| pubmed:articleTitle |
Simvastatin reduces secondary brain injury caused by cortical contusion in rats: possible involvement of TLR4/NF-kappaB pathway.
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| pubmed:affiliation |
Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. Dr.Chen@utoronto.ca
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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