Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-8-16
pubmed:abstractText
We examined the neuroprotective mechanism of cannabidiol, non-psychoactive component of marijuana, on the infarction in a 4 h mouse middle cerebral artery (MCA) occlusion model in comparison with Delta(9)-tetrahydrocannabinol (Delta(9)-THC). Release of glutamate in the cortex was measured at 2 h after MCA occlusion. Myeloperoxidase (MPO) and cerebral blood flow were measured at 1 h after reperfusion. In addition, infarct size and MPO were determined at 24 and 72 h after MCA occlusion. The neuroprotective effect of cannabidiol was not inhibited by either SR141716 or AM630. Both pre- and post-ischemic treatment with cannabidiol resulted in potent and long-lasting neuroprotection, whereas only pre-ischemic treatment with Delta(9)-THC reduced the infarction. Unlike Delta(9)-THC, cannabidiol did not affect the excess release of glutamate in the cortex after occlusion. Cannabidiol suppressed the decrease in cerebral blood flow by the failure of cerebral microcirculation after reperfusion and inhibited MPO activity in neutrophils. Furthermore, the number of MPO-immunopositive cells was reduced in the ipsilateral hemisphere in cannabidiol-treated group. Cannabidiol provides potent and long-lasting neuroprotection through an anti-inflammatory CB(1) receptor-independent mechanism, suggesting that cannabidiol will have a palliative action and open new therapeutic possibilities for treating cerebrovascular disorders.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1488-96
pubmed:meshHeading
pubmed-meshheading:17437545-Animals, pubmed-meshheading:17437545-Behavior, Animal, pubmed-meshheading:17437545-Cannabidiol, pubmed-meshheading:17437545-Cerebrovascular Circulation, pubmed-meshheading:17437545-Disease Models, Animal, pubmed-meshheading:17437545-Dose-Response Relationship, Drug, pubmed-meshheading:17437545-Functional Laterality, pubmed-meshheading:17437545-Glutamic Acid, pubmed-meshheading:17437545-Infarction, Middle Cerebral Artery, pubmed-meshheading:17437545-Male, pubmed-meshheading:17437545-Mice, pubmed-meshheading:17437545-Motor Activity, pubmed-meshheading:17437545-Neuroprotective Agents, pubmed-meshheading:17437545-Perfusion, pubmed-meshheading:17437545-Peroxidase, pubmed-meshheading:17437545-Piperidines, pubmed-meshheading:17437545-Pyrazoles, pubmed-meshheading:17437545-Receptors, Cannabinoid, pubmed-meshheading:17437545-Tetrahydrocannabinol, pubmed-meshheading:17437545-Tetrazolium Salts, pubmed-meshheading:17437545-Time Factors
pubmed:year
2007
pubmed:articleTitle
Delayed treatment with cannabidiol has a cerebroprotective action via a cannabinoid receptor-independent myeloperoxidase-inhibiting mechanism.
pubmed:affiliation
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't