Cerebral ischemia/reperfusion injury in rat brain: effects of naloxone

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Abstract
The pathogenesis of cerebral ischemia/reperfusion (I/R) involves cytokine/chemokine production, inflammatory cell influx, astrogliosis, cytoskeletal protein degradation and breakdown of the blood–brain barrier. (−)-Naloxone is able to reduce infarct volume and has been used as a therapeutic agent for cerebral I/R injuries. However, its effects on the mentioned pathophysiologic changes have scarcely been addressed. Cerebral I/R was produced by occluding and opening bilateral common carotid artery and unilateral middle cerebral artery in Sprague-Dawley rats. After cerebral I/R, the degradation of neuronal microtubule-associated protein-2 (MAP-2) was strongly associated with astrogliosis, inflammatory cell infiltration, cytokine/chemokine overproduction, and matrix metalloproteinase-9 activation. (−)-Naloxone pretreatment suppresses post-ischemic activation and preserves more MAP-2 protein. Therefore, (−)-naloxone administration might be an effective therapeutic intervention for reducing ischemic injuries.