Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/70807
DC FieldValueLanguage
dc.contributor.authorKao, T.K.en_US
dc.contributor.authorOu, Y.C.en_US
dc.contributor.authorLiao, S.L.en_US
dc.contributor.authorChen, W.Y.en_US
dc.contributor.authorWang, C.C.en_US
dc.contributor.authorChen, S.Y.en_US
dc.contributor.authorChiang, A.N.en_US
dc.contributor.authorChen, C.J.en_US
dc.date2008zh_TW
dc.date.accessioned2014-06-11T06:00:23Z-
dc.date.available2014-06-11T06:00:23Z-
dc.identifier.issn0197-0186zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/70807-
dc.description.abstractAlterations in the opioidergic system have been found in cerebral ischemia. Neuroprotection studies have demonstrated the involvement of the opioidergic system in cerebral ischemia/reperfusion (I/R). However, the neuroprotective mechanisms remain largely unclear. This study was conducted to investigate whether intracerebroventricular administration of opioidergic agonists; has a neuroprotective effect against cerebral ischemia in rats and, if this proved to be the case, to determine the potential neuroprotective mechanisms. Using a focal cerebral I/R. rat model, we demonstrated that the opioidergic agents, BW373U86 (delta agonist) and Dynorphin A 1-13 (kappa agonist), but not TAPP (mu agonist), attenuated cerebral ischemic injury as manifested in the reduction of cerebral infarction and preservation of neurons. The antagonism assay showed that the neuroprotective effect of Dynorphin A was attenuated by nor-Binaltorphimine (kappa antagonist). Surprisingly, BW373U86-induced neuroprotection was not changed by Naltrindole (delta antagonist). These findings indicate that BW373U86 and Dynorphin A exerted distinct neuroprotection against ischemia via opioid-independent and -dependent mechanisms, respectively. The post-ischemic protection in beneficial treatments was accompanied by alleviations in brain edema, inflammatory cell infiltration, and pro-inflaminatory cytokine interleukin 6 (IL-6) expression. In vitro cell study further demonstrated that the opioidergic agonists, delta and kappa, but not mu, attenuated IL-6 production from stimulated glial cells. Our findings indicate that opioidergic agents have a role in post-ischemic progression through both opioid-dependent and -independent mechanisms. In spite of the distinct-involved action mechanism, the potential neuroprotective effect of opioidergic compounds was associated with immune suppression. Taken together, these findings suggest a potential role for opioidergic agents in the therapeutic consideration of neuroinflammatory diseases. However, a better understanding of the mechanisms involved is necessary before this therapeutic potential can be realized. (C) 2008 Elsevier Ltd. All rights reserved.en_US
dc.language.isoen_USzh_TW
dc.relationNeurochemistry Internationalen_US
dc.relation.ispartofseriesNeurochemistry International, Volume 52, Issue 6, Page(s) 1256-1265.en_US
dc.relation.urihttp://dx.doi.org/10.1016/j.neuint.2008.01.007en_US
dc.subjectischemiaen_US
dc.subjectneuroinflammationen_US
dc.subjectneuroprotectionen_US
dc.subjectopiciden_US
dc.subjectstrokeen_US
dc.subjectfocal cerebral-ischemiaen_US
dc.subjectreceptor messenger-rnaen_US
dc.subjectforebrain ischemiaen_US
dc.subjectartery occlusionen_US
dc.subjectnitric-oxideen_US
dc.subjectbrain-injuryen_US
dc.subjectlipid raftsen_US
dc.subjectdeltaen_US
dc.subjectnaloxoneen_US
dc.subjectmuen_US
dc.titleOpioids modulate post-ischemic progression in a rat model of strokeen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1016/j.neuint.2008.01.007zh_TW
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en_US-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.fulltextno fulltext-
item.cerifentitytypePublications-
Appears in Collections:期刊論文
Show simple item record
 

Google ScholarTM

Check

Altmetric

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.