Linked Life Data

19925851

Source:http://linkedlifedata.com/resource/pubmed/id/19925851

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-2-1
pubmed:abstractText
The gamma isoform of protein kinase C (PKCgamma) is an injury-activated intracellular modulator that boosts neuronal activity in algesic and neuroregenerative signalling pathways. Acetyl-L-carnitine (ALCAR), a physiological compound with role in bioenergetic functions, shows an antihyperalgesic effect and at the same time can exert neuroregenerative and neuroprotective effects. Aimed to explore the link between pain and neuroregeneration, the effect of ALCAR treatment (100 mg kg(-1) i.p. twice daily for 15 days) on PKCgamma and mitogen-activated protein kinases (MAPKs) expression has been evaluated in CCI (chronic constriction injury) rats. The sciatic nerve and the lumbar tract of the spinal cord were processed to evaluate the levels of the phosphorylated form of PKCgamma, ERK 1,2, SAP/JNK, p-38 and c-Jun; furthermore, the mRNA expression of the early genes c-Jun and c-Fos has been investigated. Fifteen days after injury, the analysis in the sciatic nerves highlighted a bilateral increase of the activated forms of PKCgamma, ERK 1,2 and SAP/JNK, whereas c-Jun showed an increase only ipsilaterally. ALCAR completely prevented mechanical hyperalgesia and provoked in the nerve a c-Jun increment only. In the lumbar tract of the spinal cord, higher levels of activated PKCgamma, ERK 1,2, p38, SAP/JNK and c-Jun proteins were detected in the ipsilateral side in respect of sham. ALCAR was able to stimulate this expression profile. At the transcriptional level c-Jun mRNA was increased in the ipsilateral side of spinal cord of CCI saline-treated rats, whereas c-Fos mRNA was unchanged. ALCAR had a stimulatory effect on both these early genes. These findings may represent a different approach in the study of the complex balance between pain and neuroregeneration and could constitute the basis for developing new disease modifying agents in the treatment of neuropathic pain.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1873-7544
pubmed:author
pubmed:issnType
Electronic
pubmed:day
17
pubmed:volume
165
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1345-52
pubmed:meshHeading
pubmed-meshheading:19925851-Acetylcarnitine, pubmed-meshheading:19925851-Animals, pubmed-meshheading:19925851-Disease Models, Animal, pubmed-meshheading:19925851-Enzyme Activation, pubmed-meshheading:19925851-Functional Laterality, pubmed-meshheading:19925851-Hyperalgesia, pubmed-meshheading:19925851-Male, pubmed-meshheading:19925851-Mitogen-Activated Protein Kinases, pubmed-meshheading:19925851-Neuroprotective Agents, pubmed-meshheading:19925851-Pain, pubmed-meshheading:19925851-Protein Kinase C, pubmed-meshheading:19925851-Proto-Oncogene Proteins c-fos, pubmed-meshheading:19925851-Proto-Oncogene Proteins c-jun, pubmed-meshheading:19925851-RNA, Messenger, pubmed-meshheading:19925851-Rats, pubmed-meshheading:19925851-Rats, Sprague-Dawley, pubmed-meshheading:19925851-Sciatic Nerve, pubmed-meshheading:19925851-Sciatic Neuropathy, pubmed-meshheading:19925851-Spinal Cord
pubmed:year
2010
pubmed:articleTitle
The neuropathy-protective agent acetyl-L-carnitine activates protein kinase C-gamma and MAPKs in a rat model of neuropathic pain.
pubmed:affiliation
University of Florence, Department of Preclinical and Clinical Pharmacology, Florence, Italy. lorenzo.mannelli@unifi.it
pubmed:publicationType
Journal Article