Linked Life Data

11246166

Source:http://linkedlifedata.com/resource/pubmed/id/11246166

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-3-14
pubmed:abstractText
The expression of interleukin-1beta and tumor necrosis factor has previously been shown to be up-regulated in the spinal cord of several rat mononeuropathy models. This present study was undertaken to determine whether blocking the action of central interleukin-1beta and tumor necrosis factor attenuates mechanical allodynia in a gender-specific manner in a rodent L5 spinal nerve transection model of neuropathic pain, and whether this inhibition occurs via down-regulation of the central cytokine cascade or blockade of glial activation. Interleukin-1 receptor antagonist or soluble tumor necrosis factor receptor was administered intrathecally via lumbar puncture to male Holtzman rats in a preventative pain strategy, in which therapy was initiated 1h prior to surgery. Administration of soluble tumor necrosis factor receptor attenuated mechanical allodynia, while interleukin-1 receptor antagonist alone was unable to decrease allodynia. Interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor, administered to both male and female rats in a preventative pain strategy, significantly reduced mechanical allodynia in a dose-dependent manner (P<0.01). The magnitude of attenuation in allodynia was similar in both males and females. Immunohistochemistry on L5 spinal cord revealed similar astrocytic and microglial activation regardless of treatment. At days 3 and 7 post-transection, animals receiving daily interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor exhibited significantly less interleukin-6, but not interleukin-1beta, in the L5 spinal cord compared to vehicle-treated animals. In an existing pain paradigm, in which treatment was initiated on day 7 post-transection, interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor attenuated mechanical allodynia (P<0.05) in male rats. These findings further support a role for central interleukin-1beta and tumor necrosis factor in the development and maintenance of neuropathic pain through induction of a proinflammatory cytokine cascade.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
103
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
529-39
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11246166-Animals, pubmed-meshheading:11246166-Disease Models, Animal, pubmed-meshheading:11246166-Drug Therapy, Combination, pubmed-meshheading:11246166-Female, pubmed-meshheading:11246166-Immunoglobulin G, pubmed-meshheading:11246166-Injections, Spinal, pubmed-meshheading:11246166-Interleukin 1 Receptor Antagonist Protein, pubmed-meshheading:11246166-Interleukin-1, pubmed-meshheading:11246166-Interleukin-6, pubmed-meshheading:11246166-Male, pubmed-meshheading:11246166-Neuralgia, pubmed-meshheading:11246166-Neuroglia, pubmed-meshheading:11246166-Neurons, pubmed-meshheading:11246166-Rats, pubmed-meshheading:11246166-Rats, Sprague-Dawley, pubmed-meshheading:11246166-Receptors, Tumor Necrosis Factor, pubmed-meshheading:11246166-Sex Factors, pubmed-meshheading:11246166-Sialoglycoproteins, pubmed-meshheading:11246166-Spinal Cord, pubmed-meshheading:11246166-Spinal Nerves, pubmed-meshheading:11246166-Tumor Necrosis Factor-alpha
pubmed:year
2001
pubmed:articleTitle
Intrathecal interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor exhibits an anti-allodynic action in a rat model of neuropathic pain.
pubmed:affiliation
Department of Pharmacology and Toxicology, Hinman Box 7650, Dartmouth College, Hanover, NH 03755, USA. sarah.sweitzer@dartmouth.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't