首页> 中文期刊> 《皖南医学院学报》 >脑缺血后脑红蛋白对细胞色素C及Caspas-3的作用

脑缺血后脑红蛋白对细胞色素C及Caspas-3的作用

         

摘要

目的:观察脑缺血半暗区脑红蛋白(neuroglobin,NGB)与细胞色素C(Cyt-C)相关性,以探讨NGB在脑缺血早期是否通过Cyt-C途径抑制Caspase-3表达.方法:大鼠随机分为假手术对照组(Sham)、缺血再灌注组(CIR)、干预组(IV)和干预对照组(IVC).CIR组制作脑缺血再灌注模型,按断头时程不同又分为1 h、6 h、12 h、24 h、72 h 5个亚组.IV组将重组人NGB注入左侧尾壳核30 min后制作脑缺血再灌注模型,按断头时程不同又分为1 h、6 h、12 h、24 h、72 h 5个亚组,其中Sham组和IVC组于24 h断头.取脑作HE和免疫组化染色.结果:NGB在缺血再灌注1h已经升高,24 h后达高峰,然后逐步下降.Caspase-3和 Cyt-C 在1 h后表达增多,12~24 h增高达到高峰,然后逐步下降.干预后Cyt-C表达明显减少(P<0.01),Caspase-3表达也明显减少(P<0.05).结论:脑缺血后NGB在缺血半暗区先升高后下降,可能通过Cyt-C途径抑制Caspas-3表达而发挥脑保护作用.%Objective: To find out whether neuroglobin (NGB) could regulate caspase-3 expression through pathway of cytochrome(Cyt-C) in penumbra after cerebral ischemia reperfusion by examining the correlation of the two factors.Methods: Seventy-two male Sprague-Dawley ( SD ) rats were randomized into groups of sham operation(Sham) ,cerebral ischemia-reperfusion ( CIR ), intervention ( Ⅳ ) and interventional controls (IVC).After CIR models were developed, the rats were decapitated and subgrouped chronologically into CIR of 1 h,6 h,12 h,24 h and 72 h,respectively.In Ⅳ group, CIR models were established 30 min after injection of recombinant human NGB into the left striatum, followed by subgrouping chronologically into CIR of 1 h,6 h, 12 h,24 h and 72 h, respectively.The animals in both Sham and IVC were killed at 24 h.Cerebral specimens were obtained for section with HE and immunohistostaining.Results:NGB expression was found up-regulated at 1h after CIR and peaked at 24 h before it down-regulating progressively.Increased expression was seen at 1h for caspase-3 and Cyt-C, topping at 12 ~24 h and descendeing thereafter.After injection of recombinant human NGB into the left striatum, expression of Cyt-C and caspase-3 was seen down-graded significantly ( P < 0.01, P < 0.05 ).Conclusion: NGB was increased before fall in ischemic penumbra after cerebral ischemia-reperfusion, suggesting that NGB may be involved in the neuroprotection by inhibiting caspas-3 expression through pathway of Cyt-C.

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