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In this study, we assessed the effect of EA pretreatment on the expression of \u03b17 nicotinic acetylcholine receptors (\u03b17nAChR), using the ischemia-reperfusion model of focal cerebral ischemia in rats. Further, we investigated the role of high mobility group box 1 (HMGB1) in neuroprotection mediated by the \u03b17nAChR and EA.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>Rats were treated with EA at the acupoint \"Baihui (GV 20)\" 24 h before focal cerebral ischemia which was induced for 120 min by middle cerebral artery occlusion. Neurobehavioral scores, infarction volumes, neuronal apoptosis, and HMGB1 levels were evaluated after reperfusion. The \u03b17nAChR agonist PHA-543613 and the antagonist \u03b1-bungarotoxin (\u03b1-BGT) were used to investigate the role of the \u03b17nAChR in mediating neuroprotective effects. The roles of the \u03b17nAChR and HMGB1 release in neuroprotection were further tested in neuronal cultures exposed to oxygen and glucose deprivation (OGD).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Our results showed that the expression of \u03b17nAChR was significantly decreased after reperfusion. EA pretreatment prevented the reduction in neuronal expression of \u03b17nAChR after reperfusion in the ischemic penumbra. Pretreatment with PHA-543613 afforded neuroprotective effects against ischemic damage. Moreover, EA pretreatment reduced infarct volume, improved neurological outcome, inhibited neuronal apoptosis and HMGB1 release following reperfusion, and the beneficial effects were attenuated by \u03b1-BGT. The HMGB1 levels in plasma and the penumbral brain tissue were correlated with the number of apoptotic neurons in the ischemic penumbra. Furthermore, OGD in cultured neurons triggered HMGB1 release into the culture medium, and this effect was efficiently suppressed by PHA-543,613. Pretreatment with \u03b1-BGT reversed the inhibitory effect of PHA-543,613 on HMGB1 release.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>These data demonstrate that EA pretreatment strongly protects the brain against transient cerebral ischemic injury, and inhibits HMGB1 release through \u03b17nAChR activation in rats. These findings suggest the novel potential for stroke interventions harnessing the anti-inflammatory effects of \u03b17nAChR activation, through acupuncture or pharmacological strategies.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1742-2094-9-24","type":"journal-article","created":{"date-parts":[[2012,1,26]],"date-time":"2012-01-26T07:23:54Z","timestamp":1327562634000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":98,"title":["Electroacupuncture pretreatment attenuates cerebral ischemic injury through \u03b17 nicotinic acetylcholine receptor-mediated inhibition of high-mobility group box 1 release in 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