Abstract：Objective: To study the protective effect and mechanism of dexmedetomidine (Dex) after treatment in rats with focal cerebral ischemia- reperfusion injury. Methods:A total of 120 healthy Sprague-Dawley (SD) rats were randomly divided into the sham operation group (S group), ischemia reperfusion group (Mod group), dexmedetomidine pretreatment group (Dex1 group, treated with abdominal injection of 50μg/kg Dex of 100μg/mL at 30min before making MCAO models) and dexmedetomidine after treatment group (Dex2 group, treated with intraperitoneal injection of 50μg/kg Dex of 100μg/mL immediately after reperfusion), with 30 rats in each group. Except S group, 24h after ischemia reperfusion, the neurological function (bederson) score was compared between the other groups, the volume of cerebral infarction was determined by TTC staining method, the percentage of infarct was calculated, and levels of neuron specific enolase (NSE), superoxide dismutase (SOD) and malondialdehyde (MDA) were determined by enzyme-linked immunosorbent assay, xanthine oxidase method and thiobarbituric acid method. The expression quantities of response element binding protein (CREB), Bcl-2 and brain-derived neurotrophic factor (BNDF) mRNA and protein in all groups were detected by RT-PCR method and Western blot method. The immunoenzyme labeling assay (SP) was used for immunohistochemical staining. Results:There was no significant difference of bederson score between Mod group and Dex1 group, but bederson scores of Mod group and Dex1 group were significantly higher than those of Dex2 group. TTC staining showed that the infarct volume and the percentage of infarct volume in total brain volume in Dex1 group and Mod group were significantly higher than those in Dex2 group. Levels of NSE and MDA in Dex2 group were significantly lower than those in Dex1 group while the SOD level was significantly higher than that in Dex1 group. RT-PCR, Westernblot and immunohistochemical analysis showed that expression quantities and positive expression rates of CREB, Bcl-2 and BDNF mRNA and protein in Dex2 group were higher than those in Mod group and Dex1 group, showing Dex2 group > Dex1 group > Mod group (P < 0.05). Conclusion:Dexmedetomidine has certain protective effect in rats with ischemia reperfusion injury. Dexmedetomidine after treatment can enhance the activities of autioxidant enzymes and inhibit oxidative stress reactions in rats with focal cerebral ischemia reperfusion. It also can improve the expression of Bcl-2 and BDNF through regulating response element binding protein (CREB) of cyclic adenosine monophosphate. The protective effect on brain is significant.
曹立梅, 李强, 董智强, 陈旭. 右美托咪定后处理对大鼠局灶性脑缺血-再灌注损伤的保护作用及机制研究[J]. 河北医学, 2018, 24(5): 705-710.
CAO Limei, LI Qiang, DONG Zhiqiang, et al. The Protective Effect and Mechanism of Dexmedetomidine after Treatment in Rats with Focal Cerebral Ischemia- reperfusion Injury. HeBei Med, 2018, 24(5): 705-710.
2018, Vol. 24 
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