红花注射液对脑缺血再灌注损伤大鼠大脑皮质Bax及Bcl-XL/Bcl-2的影响

Inf luence of Saff lower Injection on Expression of Bax and Bcl-XL/Bcl-2 Protein in the Cortex of Rat after IschemiaReperfusion Injury

目的:以大鼠脑缺血再灌注损伤模型为研究对象,探讨红花注射液对大鼠大脑皮质B细胞淋巴瘤-2(B-cell leukemia-2,Bcl-2)蛋白、Bcl-2相关X蛋白(Bcl-2 associated x protein,Bax)、Bcl-XL(B-cell lymphomaextra large)蛋白表达的影响。方法:健康成年雄性SD大鼠30只,随机分为6组,分别为假手术组(生理盐水1.6 m L·kg-1),模型组(生理盐水1.6 m L·kg-1),红花注射液低剂量组(0.8 m L·kg-1)、中剂量组(1.6 m L·kg-1)、高剂量组(3.2 m L·kg-1)及尼莫地平组(2.0 m L·kg-1)。采用线栓法建立大鼠局灶性脑缺血再灌注损伤模型,采用免疫组织化学方法检测大鼠脑皮质Bax、Bcl-2、Bcl-XL蛋白的表达。结果:模型组脑组织缺血周边区域中Bax、Bcl-2、Bcl-XL阳性细胞表达较假手术组明显增加(P<0.05);而与模型组比较,红花注射液低、中、高剂量组和尼莫地平注射液组脑组织缺血周边区域中Bax阳性细胞表达明显减少(P<0.05),而Bcl-2、Bcl-XL阳性细胞表达均明显增加(P<0.05)。结论:红花注射液可通过增加Bcl-2、Bcl-XL蛋白及下调Bax蛋白的表达减少大脑神经细胞凋亡,对缺血再灌注损伤大鼠脑组织发挥保护作用。

Objective：To explore the influence of safflower injection on expression of Bax, Bcl-2 and Bcl-XL protein in the cortex of rat after ischemia-reperfusion injury. Methods：30 healthy male SD rats were randomly divided into six groups,as indicated,control group,model control group,safflower injection low dose group（0.8 m L·kg（-1））,middle dose group（1.6 m L·kg（-1））,high dose group（3.2 m L·kg（-1）） and Nimodipine group（2.0 m L·kg（-1））. The focal cerebral ischemia-reperfusion injury model was established by thread technique,and the expression of Bax,Bcl-2 and Bcl-XL protein in the rat brain cortex was detected through immunohistochemical methods. Results：We found that the expression of positive cells of Bax,Bcl-2 and Bcl-XL protein was signifi cantly increased in the surrounding area of the ischemic brain tissue in the model group,compared with the control group（P0.05）; and the expression of positive cells of Bax protein was reduced and the expression of Bcl-2,Bcl-XL protein was rised in the surrounding area of the ischemic brain tissue in the safflower injection low dose group,middle dose group,high dose group and Nimodipine group,compared with the model group（P0.05）. Conclusion：Safflower injection can protect cerebral neurons from apoptosis through augmenting the expresson of Bcl-2,Bcl-XL and decreasing the expression of Bax protein after ischemia-reperfusion injury.