Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-11-19
pubmed:abstractText
We have previously shown that honokiol, an active component of Magnolia officinalis, displayed protective effect against focal cerebral ischemia-reperfusion (FCI/R) injury in rats. Production of reactive oxygen species (ROS) and infiltration of neutrophils to injured tissue play deleterious roles during cerebral ischemia. To study the mechanism(s) in mediating neuroprotective effect of honokiol, FCI/R-induced neutrophil infiltration and lipid peroxidation in brain tissue, and activation of neutrophils in-vitro were examined. Intravenous administration of honokiol (0.01-1.0 microg/kg) 15 min before (pretreatment) or 60 min after (post-treatment) middle cerebral artery occlusion reduced the total infarcted volume by 20-70% in dose-dependent manner. Pretreatment or post-treatment of honokiol at concentration of 0.1 and 1.0 microg/kg significantly decreased the neutrophil infiltration in the infarcted brain. Time course of neutrophil infiltration was performed in parallel with the lipid peroxidation in infracted brain tissue during FCI/R injury. The results indicate that honokiol can protect brain tissue against lipid peroxidation and neutrophil infiltration during FCI/R injury and cerebral infarction induced by FCI/R is accompanied with a prominent neutrophil infiltration to the infarcted area during FCI/R course. In-vitro, honokiol (0.1-10 microM) significantly diminished fMLP (N-formyl-methionyl-leucyl-phenylalanine)- or PMA (phorbol-12-myristate-13-acetate)-induced neutrophil firm adhesion, a prerequisite step behind neutrophil infiltration, and ROS production in neutrophils. Intracellular calcium overloading activates calcium-stimulated enzymes and further exaggerates FCI/R injury. Honokiol (0.1-10 microM) impeded the calcium influx induced by fMLP (a receptor agonist), AlF(4)(-) (a G-protein activator) or thapsigargin (an intracellular calcium pool releaser). Therefore, we conclude that the amelioration of FCI/R injury by honokiol can be attributed to its anti-oxidative and anti-inflammatory actions through, at least in part, limiting lipid peroxidation and reducing neutrophil activation/infiltration by interfering firm adhesion, ROS production, and calcium overloading that may be primed/activated during FCI/R injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
992
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
159-66
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:14625055-Animals, pubmed-meshheading:14625055-Biphenyl Compounds, pubmed-meshheading:14625055-Brain Ischemia, pubmed-meshheading:14625055-Calcium, pubmed-meshheading:14625055-Calcium Signaling, pubmed-meshheading:14625055-Cell Adhesion, pubmed-meshheading:14625055-Cerebral Infarction, pubmed-meshheading:14625055-Chemotaxis, Leukocyte, pubmed-meshheading:14625055-Dose-Response Relationship, Drug, pubmed-meshheading:14625055-Infarction, Middle Cerebral Artery, pubmed-meshheading:14625055-Lignans, pubmed-meshheading:14625055-Lipid Peroxidation, pubmed-meshheading:14625055-Male, pubmed-meshheading:14625055-N-Formylmethionine Leucyl-Phenylalanine, pubmed-meshheading:14625055-Neuroprotective Agents, pubmed-meshheading:14625055-Neutrophils, pubmed-meshheading:14625055-Rats, pubmed-meshheading:14625055-Rats, Long-Evans, pubmed-meshheading:14625055-Reactive Oxygen Species, pubmed-meshheading:14625055-Reperfusion Injury, pubmed-meshheading:14625055-Tetradecanoylphorbol Acetate
pubmed:year
2003
pubmed:articleTitle
Honokiol protects rat brain from focal cerebral ischemia-reperfusion injury by inhibiting neutrophil infiltration and reactive oxygen species production.
pubmed:affiliation
Institute of Clinical Medicine, National Yang-Ming University School of Medicine, Taipei, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't