Neuroprotection of Dexmedetomidine against Cerebral Ischemia-Reperfusion Injury in Rats: Involved in Inhibition of NF-κB and Inflammation Response
Biomolecules & Therapeutics
;
: 383-389, 2017.
Article
in English
| WPRIM
| ID: wpr-129206
ABSTRACT
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Brain Edema
/
RNA, Messenger
/
Reperfusion
/
Reperfusion Injury
/
Cytokines
/
Interleukin-6
/
Rats, Sprague-Dawley
/
Infarction, Middle Cerebral Artery
/
Dexmedetomidine
/
Cyclooxygenase 2
Limits:
Animals
Language:
English
Journal:
Biomolecules & Therapeutics
Year:
2017
Type:
Article
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