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目的探讨丁基苯酞(NBP)对大鼠脑缺血再灌注损伤后Bcl-2蛋白和mRNA表达的影响。方法利用大脑中动脉线栓法建立大鼠局灶性缺血再灌注模型,随机分为假手术组(不阻断大脑中动脉)、脑缺血再灌注组(I/R组)和NBP治疗组(NBP组);脑缺血2 h后开始再灌注。NBP组ig 25 mg.kg-1 NBP,每天2次,I/R组及假手术组ig相同剂量食用植物油。再灌注72 h后,行神经功能缺损评分,然后断头取脑,用TTC染色观察脑梗死体积,免疫组织化学法检测梗死核心区、梗死周围区、海马区Bcl-2蛋白的表达,原位杂交法检测Bcl-2 mRNA的表达。结果 NBP组较I/R组大鼠脑梗死体积小(P<0.05),神经功能缺损改善(P<0.05);梗死核心区NBP组和I/R组Bcl-2蛋白和mRNA表达差异无统计学意义(P>0.05),NBP组在梗死周围区和海马区的Bcl-2蛋白和mRNA表达均高于I/R组和假手术组(P<0.05)。结论 NBP可减少脑缺血再灌注后大鼠脑梗死的体积,改善神经功能,促进大鼠脑梗死周围区和海马区Bcl-2蛋白和mRNA的表达,可能为NBP抗凋亡和保护缺血脑组织的机制之一。
Objective To investigate the effect of butylphthalide (NBP) on the expression of Bcl-2 protein and mRNA after cerebral ischemia-reperfusion injury in rats. Methods The model of focal ischemia-reperfusion in rats was established by the method of middle cerebral artery occlusion (MCAO). The rats were randomly divided into sham-operated group (without blocking middle cerebral artery), cerebral ischemia-reperfusion group (I / R group) Group (NBP group); reperfusion was started 2 h after cerebral ischemia. NBP group ig 25 mg.kg-1 NBP, 2 times a day, I / R group and sham group ig the same dose of edible vegetable oil. After 72 h of reperfusion, the neurological deficit scores were scored and the brain was decapitated. The volume of cerebral infarction was observed by TTC staining. The expression of Bcl-2 protein in infarct core area, infarct area and hippocampus area was detected by immunohistochemistry. Hybridization method was used to detect the expression of Bcl-2 mRNA. Results Compared with I / R group, NBP group had smaller infarction size (P <0.05) and improved neurological deficit (P <0.05). There was no statistical difference in the expression of Bcl-2 protein and mRNA in NBP group and I / R group (P> 0.05). The expressions of Bcl-2 protein and mRNA in NBP group were higher than those in I / R group and sham operation group (P <0.05). Conclusion NBP can decrease the volume of cerebral infarction, improve the neurological function and promote the expression of Bcl-2 protein and mRNA in the peri-infarct and hippocampus of rats after cerebral ischemia and reperfusion, which may be the result of NBP anti-apoptosis and protection of ischemia One of the mechanisms of brain tissue.