Neuroprotection of Dexmedetomidine against Cerebral Ischemia-Reperfusion Injury in Rats: Involved in Inhibition of NF-κB and Inflammation Response

التفاصيل البيبلوغرافية
العنوان: Neuroprotection of Dexmedetomidine against Cerebral Ischemia-Reperfusion Injury in Rats: Involved in Inhibition of NF-κB and Inflammation Response
المؤلفون: Li-gong Zhang, Lijun Wang, Haiyan Liu, Yonghui Yu, Meng-yuan Zhang, Gongming Wang
المصدر: Biomolecules & Therapeutics
بيانات النشر: The Korean Society of Applied Pharmacology, 2017.
سنة النشر: 2017
مصطلحات موضوعية: 0301 basic medicine, Agonist, medicine.drug_class, Ischemia, Inflammation, Pharmacology, Cerebral ischemia-reperfusion, Biochemistry, Neuroprotection, Proinflammatory cytokine, 03 medical and health sciences, 0302 clinical medicine, Drug Discovery, medicine, Cyclooxygenase-2, Dexmedetomidine, Inducible nitric oxide synthase, biology, business.industry, Nuclear factor-κB, medicine.disease, Nitric oxide synthase, 030104 developmental biology, Anesthesia, biology.protein, Molecular Medicine, Original Article, medicine.symptom, business, Reperfusion injury, 030217 neurology & neurosurgery, medicine.drug
الوصف: 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.
تدمد: 1976-9148
2005-4483
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8fd2b67f07ce74453fc46e25eece931a
https://doi.org/10.4062/biomolther.2015.180
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....8fd2b67f07ce74453fc46e25eece931a
قاعدة البيانات: OpenAIRE