Linked Life Data

10779657

Source:http://linkedlifedata.com/resource/pubmed/id/10779657

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2000-6-30
pubmed:abstractText
Inflammatory mechanisms are believed to play an important role in hyperalgesia resulting from nerve injury. Hyperalgesia following nerve injury is temporally linked with Wallerian degeneration and macrophage recruitment, and is reduced in WLD mice, in which Wallerian degeneration is delayed. We sought more direct evidence that macrophages contribute to hyperalgesia and Wallerian degeneration by depleting macrophages with liposomes loaded with dichloromethylene diphosphonate (clodronate, Cl(2)MDP). Rats were subjected to partial ligation of the sciatic nerve. Intravenous injection of liposome-encapsulated clodronate reduced the number of macrophages in the injured nerve, alleviated thermal hyperalgesia and protected both myelinated and unmyelinated fibres against degeneration. The results confirm the role of circulating monocytes/macrophages in the development of neuropathic hyperalgesia and Wallerian degeneration due to partial nerve injury. Macrophage depletion immediately after nerve injury could have some clinical potential in prevention of neuropathic pain.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0304-3959
pubmed:author
pubmed:issnType
Print
pubmed:volume
86
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
25-32
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Depletion of macrophages reduces axonal degeneration and hyperalgesia following nerve injury.
pubmed:affiliation
School of Anatomy, University of New South Wales, Sydney, Australia.
pubmed:publicationType
Journal Article