Biomol Ther (Seoul)  
Neuroprotection of Dexmedetomidine against Cerebral Ischemia-Reperfusion Injury in Rats: Involved in Inhibition of NF-κB and Inflammation Response
Lijun Wang1,†, Haiyan Liu1,†, Ligong Zhang2,*, Gongming Wang2, Mengyuan Zhang2 and Yonghui Yu1
Departments of 1Pediatrics, 2Anesthesia, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China
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The first two authors contributed equally to this work.
Received: November 9, 2015; Revised: May 9, 2016; Accepted: September 21, 2016; Published online: November 25, 2016.
© The Korean Society of Applied Pharmacology. All rights reserved.

Dexmedetomidine is an α2-adrenergic receptor agonist that exhibits a protective effect on ischemia-reperfusion injury of the heart, kidney, and other organs. In the present study, we examined the neuroprotective action and potential mechanisms of dexmedetomidine against ischemia-reperfusion induced cerebral injury. Transient focal cerebral ischemia-reperfusion injury was induced in Sprague-Dawley rats by middle cerebral artery occlusion. After the ischemic insult, animals then received intravenous dexmedetomidine of 1 µg/kg load dose, followed by 0.05 µg/kg/min infusion for 2 h. After 24 h of reperfusion, neurological function, brain edema, and the morphology of the hippocampal CA1 region were evaluated. The levels and mRNA expressions of interleukin-1β, interleukin-6 and tumor nevrosis factor-α as well as the protein expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-κBp65, inhibitor of κBα and phosphorylated of κBα in hippocampus were assessed. We found that dexmedetomidine reduced focal cerebral ischemia-reperfusion injury in rats by inhibiting the expression and release of inflammatory cytokines and mediators. Inhibition of the nuclear factor-κB pathway may be a mechanism underlying the neuroprotective action of dexmedetomidine against focal cerebral I/R injury.
Keywords: Cerebral ischemia-reperfusion, Dexmedetomidine, Inflammation, Inducible nitric oxide synthase, Cyclooxygenase-2, Nuclear factor-κB

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