Linked Life Data

17254027

Source:http://linkedlifedata.com/resource/pubmed/id/17254027

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-2-23
pubmed:abstractText
Evidence suggests that chronic inflammation, mitochondrial dysfunction, and oxidative stress play significant and perhaps synergistic roles in Parkinson's disease (PD), where the primary pathology is significant loss of the dopaminergic neurons in the substantia nigra. The use of anti-inflammatory drugs for PD treatment has been proposed, and inhibition of cyclo-oxygenase-2 (COX-2) or activation of peroxisome proliferator-activated receptor gamma (PPAR-gamma) yields neuroprotection in MPTP-induced PD. Lipopolysaccharide (LPS) induces inflammation-driven dopaminergic neurodegeneration. We tested the hypothesis that celecoxib (Celebrex, COX-2 inhibitor) or pioglitazone (Actos, PPAR-gamma agonist) will reduce the LPS-induced inflammatory response, spare mitochondrial bioenergetics, and improve nigral dopaminergic neuronal survival. Rats were treated with vehicle, celecoxib, or pioglitazone and were intrastriatally injected with LPS. Inflammation, mitochondrial dysfunction, oxidative stress, decreased dopamine, and nigral dopaminergic neuronal loss were observed post-LPS. Celecoxib and pioglitazone provided neuroprotective properties by decreasing inflammation and restoring mitochondrial function. Pioglitazone also attenuated oxidative stress and partially restored striatal dopamine as well as demonstrated dopaminergic neuroprotection and reduced nigral microglial activation. In summary, intrastriatal LPS served as a model for inflammation-induced dopaminergic neurodegeneration, anti-inflammatory drugs provided protective properties, and pioglitazone or celecoxib may have therapeutic potential for the treatment of neuro-inflammation and PD.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
100
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1375-86
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17254027-Animals, pubmed-meshheading:17254027-Cell Death, pubmed-meshheading:17254027-Corpus Striatum, pubmed-meshheading:17254027-Cyclooxygenase 2 Inhibitors, pubmed-meshheading:17254027-Dopamine, pubmed-meshheading:17254027-Inflammation, pubmed-meshheading:17254027-Lipopolysaccharides, pubmed-meshheading:17254027-Male, pubmed-meshheading:17254027-Microglia, pubmed-meshheading:17254027-Mitochondria, pubmed-meshheading:17254027-Nerve Degeneration, pubmed-meshheading:17254027-Neurons, pubmed-meshheading:17254027-PPAR gamma, pubmed-meshheading:17254027-Pyrazoles, pubmed-meshheading:17254027-Rats, pubmed-meshheading:17254027-Rats, Sprague-Dawley, pubmed-meshheading:17254027-Receptor, Insulin, pubmed-meshheading:17254027-Substantia Nigra, pubmed-meshheading:17254027-Sulfonamides, pubmed-meshheading:17254027-Thiazolidinediones
pubmed:year
2007
pubmed:articleTitle
Inflammation induces mitochondrial dysfunction and dopaminergic neurodegeneration in the nigrostriatal system.
pubmed:affiliation
Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky 40536-0298, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural