KMID : 0606920170250040383
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Biomolecules & Therapeutics 2017 Volume.25 No. 4 p.383 ~ p.389
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Neuroprotection of Dexmedetomidine against Cerebral Ischemia-Reperfusion Injury in Rats: Involved in Inhibition of NF-¥êB and Inflammation Response
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Wang Li Jun
Liu Hai Yan Zhang Li Gong Wang Gong Ming Zhang Meng Yuan Yu Yong Hui
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Abstract
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Dexmedetomidine is an ¥á2-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 ¥ìg/kg load dose, followed by 0.05 ¥ìg/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-1¥â, interleukin-6 and tumor nevrosis factor-¥á as well as the protein expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-¥êBp65, inhibitor of ¥êB¥á and phosphorylated of ¥êB¥á 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-¥êB pathway may be a mechanism underlying the neuroprotective action of dexmedetomidine against focal cerebral I/R injury.
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KEYWORD
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Cerebral ischemia-reperfusion, Dexmedetomidine, Inflammation, Inducible nitric oxide synthase, Cyclooxygenase-2, Nuclear factor-¥êB
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