| Objective To evaluated the effects of dexmedetomidine on serum S100B protein andthe expression of TNF-α and ICAM-1in rats brain tissue after cerebral ischemia–reperfusion injury.Methods Thirty-six male rats were randomly divided into three groups: control group,intravenous saline group and intravenous dexmedetomidine group. For saline group anddexmedetomidine group rats, they were prepared for cerebral ischemia reperfusion modelusing the intraluminal thread method, while control group rats were only separated theright common carotid artery.9μg kg1dexmedetomidine was infused to thedexmedetomidine group in embolization immediately and the same capacity of sodiumchloride was infused to the saline group. Every group according to reperfusion time wasdivided into three subgroups, in24ã€48and72h after reperfusion. The scores ofneurological deficits were evaluated. The concentrations of S100B protein in serum weremeasured by ELISA method. The expression of TNF-α and ICAM–1were counted byimmunohistochemical method in the rat optic chiasma tissue.Results The Ludmila Belayev scoreã€the concentrations of S100B proteinã€the numberof TNF-α positive cells and ICAM-1positive blood vessels in dexmedetomidine groupwere significantly decreased than the saline group (F=364.348, p=0.000;F=53.274, p=0.000;F=61.748, p=0.000respectively). In saline group and dexmedetomidine group,the concentrations of S100B protein in72h after ischemia reperfusion, significantlyincreased than24h after ischemia reperfusion (F=5.195, p=5.195);The number ofTNF-α positive cells in48and72h after ischemia reperfusion were significantly decreased than24h after ischemia reperfusion (F=8.744, p=8.744); Different timepoints after ischemia-reperfusion ICAM-1positive blood vessels for there were nosignificant difference (F=1.723, p=1.723).Conclusion Small doses of dexmedetomidine has a cerebral protective effect againstischemia-reperfusion injury in the rat optic chiasma tissue; The cerebral protective effectof dexmedetomidine may be relevant to the inhibition of cytokine(TNF-α and ICAM-1)expression after cerebral injury. |