Neuroprotection of Dexmedetomidine against Cerebral Ischemia-Reperfusion Injury in Rats: Involved in Inhibition of NF-κB and Inflammation Response.
10.4062/biomolther.2015.180
- Author:
Lijun WANG
1
;
Haiyan LIU
;
Ligong ZHANG
;
Gongming WANG
;
Mengyuan ZHANG
;
Yonghui YU
Author Information
1. Departments of Pediatrics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
- Publication Type:Original Article
- Keywords:
Cerebral ischemia-reperfusion;
Dexmedetomidine;
Inflammation;
Inducible nitric oxide synthase;
Cyclooxygenase-2;
Nuclear factor-κB
- MeSH:
Animals;
Brain Edema;
CA1 Region, Hippocampal;
Cyclooxygenase 2;
Cytokines;
Dexmedetomidine*;
Heart;
Hippocampus;
Infarction, Middle Cerebral Artery;
Inflammation*;
Interleukin-6;
Kidney;
Neuroprotection*;
Nitric Oxide Synthase Type II;
Rats*;
Rats, Sprague-Dawley;
Reperfusion;
Reperfusion Injury*;
RNA, Messenger
- From:Biomolecules & Therapeutics
2017;25(4):383-389
- CountryRepublic of Korea
- Language:English
-
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.
