论文部分内容阅读
[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将♂SD大鼠建立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),每组20只大鼠;脑缺血2h后开始再灌注。NBP组每天2次灌胃NBP,每次25mg/kg,I/R组及假手术组灌胃相同剂量食用植物油。再灌注72h后行神经功能缺损评分,然后断头取脑,TTC染色观察脑梗死体积,免疫组织化学(SP)方法检测梗死核心区、梗死周围区、海马区Bcl-2蛋白的表达,原位杂交方法(POD法)检测Bcl-2mRNA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),梗死周围区和海马区NBP组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减少脑缺血再灌注后大鼠脑梗死体积,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 focal ischemia reperfusion model was established in male SD rats by middle cerebral artery occlusion method and randomly divided into sham-operated group (without blocking middle cerebral artery), cerebral ischemia-reperfusion group (I / R Group) and NBP group (NBP group), 20 rats in each group. Reperfusion was started 2h after cerebral ischemia. The NBP group was given intragastric administration of NBP twice a day for 25mg / kg, and the same dose of edible vegetable oil was given to the I / R group and the sham operation group. The neurological deficit score was measured 72h after reperfusion, then the brain was decapitated and 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 (SP) Hybridization method (POD method) to detect the expression of Bcl-2mRNA. [Results] Compared with I / R group, the infarct volume of NBP group was smaller (P <0.05) and neurological deficit was improved (P <0.05). The expression of Bcl-2 protein and mRNA in NBP group and I / R group There was no statistical significance (P> 0.05). The expressions of Bcl-2 protein and mRNA in NBP group and infarct 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 nerve 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.