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依达拉奉对大鼠脑缺血-再灌注损伤的神经保护作用 被引量:5

Neuroprotective Effects of the Antioxidant Edaravone in Rats with Cerebral Ischemia-reperfusion Injury
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摘要 目的研究自由基清除剂依达拉奉对大鼠脑缺血-再灌注损伤的神经保护作用,方法采用线栓法制备大鼠大脑中动脉缺血-再灌注模型,将SD大鼠分为再灌注组和依达拉奉组,再灌注组和依达拉奉组按再灌注2,6,12,24,48h分为5个组,依达拉奉组在缺血2h后解除栓塞,给依达拉奉3mg·kg^-1静脉注射,首次给药24h后相同剂量再次给药,再灌注组给予0.9%氯化钠溶液,给药剂量、实践和方法同依达拉奉组,检测各组血清丙二醛(MDA)浓度,免疫组化染色及原住细胞凋亡检测法(TUNEL法)测定脑系组织bcl-2蛋白表达扣凋亡细胞数,并测量各组脑梗死体积,结果依达拉奉组再灌注后6,12,24,48h的梗死体积血清MDA浓度TUNEL阳性细胞数均明显小于再灌注组(P〈0.05),各时间点bcl-2蛋白均高于再灌注组(P〈0.01),结论依达拉奉可以降低羟自由基水平,对抗细胞凋亡,对脑缺血-灌注损伤大鼠神经有明显保护作用. Objective To study the neuroprotective effects of the antioxidant Edaravone in rats with cerebral ischemia-reperfusion(IR) injury. Methods EGSD rats were randomly divided into 2 groups: the sham operation ischemia-reperfusion group and Edaravone group. Two groups were further divided into 2,6,12,24 and 48 hours subgroups according to the time of reperfusion. Edaravone group was given an injection of 3 mg·kg^-1 of Edaravone following 2 hours ischemia. 24 h later a second injection of the same dose of Edaravone was given to each of the rats of group by the same route. Another group was given 0.9% physiologic salt solution at the same time and manner as Edaravone group. The serum concentration of(MAD) was determined with the colorimetric method. Bcl-2 immunohistochemical method and TUNEL staining were used to determine the expression of the bcl-2 protein and number of TUNEL-positive apoptotic cells in the brain tissue. Results After 6,12,24 and 48 hours the serum MDA concentrations in Edaravone group were significantly lower than those of another group(P〈0.05). In addition, there was an evident increase in the expression of bcl-2 protein(P〈 0.01). Conclusion Edaravone has an excellent neuroprotective effect in rats with ischemia-reperfusion brain injury, scavenging free radicals and a bcl-2dependent anti-apoptotic mechanism.
出处 《北华大学学报(自然科学版)》 CAS 2007年第5期402-404,共3页 Journal of Beihua University(Natural Science)
关键词 依达拉奉 再灌注损伤 细胞凋亡 Edaravone Reperfusion injury Apoptosis
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  • 1[1]Roebuck KA.Oxidant Stress Regulation of IL-8 and ICA-M-1 Gene Expression:Differential Activation and Binding of the Transcription Factors AP-1 and NF-kappa B[J].Int J Mol Med,1999,4(3):223-230.
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