依达拉奉对兔脑出血后血肿周围组织中Bax及Bcl-2蛋白表达的影响

Edaravone down-regulates Bax but up-regulates Bcl-2 in rabbits after intracerebral hemorrhage

目的动态观察依达拉奉对兔脑出血后血肿周围脑组织中Bax及Bcl-2蛋白表达的影响,初步探讨依达拉奉抑制神经细胞凋亡的作用机制。方法 54只健康家兔分为实验组、假手术组以及依达拉奉干预组,通过自体血注入法建立兔脑出血模型,分别用免疫组化法及Western blot检测造模后第1、3天及第5天各组血肿周围组织Bax及Bcl-2蛋白的表达。结果免疫组化结果显示:在假手术组中,Bax和Bcl-2蛋白的表达水平较低且各时相点均无明显差异(P>0.05);实验组各时相点Bax的阳性细胞平均数均高于假手术组(P<0.01);依达拉奉干预后各时相点Bax阳性细胞平均数高于假手术组(P<0.01),但低于实验组(P<0.01)。实验组各时相点Bcl-2的阳性细胞平均数高于假手术组(P<0.01),使用依达拉奉干预后Bcl-2阳性细胞明显增多,均高于假手术组和实验组(P<0.01)。Western blot检测也得到了同样的变化趋势。结论依达拉奉抗神经细胞凋亡的作用机制可能与其下调Bax蛋白,上调Bcl-2蛋白的表达有关。

Objective To determine the role of edaravone in regulating the expression of Bax and Bcl-2 proteins in the cerebral tissue around hematoma induced by intracerebral hemorrhage in rabbits. Methods Fifty-four rabbits were randomly divided into 3 groups： sham surgery group （n = 18 ） , model group （n = 18 ）, and treatment group （n = 18）. Each group was further divided into 3 subgroups respectively： day 1 group （ n = 6）, day 3 group （ n = 6）, and day 5 group （ n = 6）. Intracerebral hemorrhage model was made by injec-ting the self-body blood to the brain of the rabbits. Expression of Bax and Bcl-2 proteins in the cerebral tissue around hematoma were analyzed by immunohistochemistry and Western blot analysis. Results In sham surgery group, immunohistochemiscal assay indicated that no significant difference was found in the expression of Bax and Bc]-2 at the different time points （P 〉 0. 05 ）. In model group, the positive expression of Bax was higher than those in the sham surgery group （P 〈 0. 01 ）. In the treatment group, the expression was higher than those in the sham surgery group （P 〈0. 01 ）, but lower than those in the model group （P 〈0. 01 ）. The expression of Bcl-2 was higher in the model group than those in the sham surgery group （ P 〈 O. 01 ）, and that in the treat- ment group was significantly higher than those in the sham surgery group and the model group （ P 〈 0.01 ）. These results were further confirmed by Western blot analysis. Conclusion Edaravone prevents the neuronal apoptosis after intracerebral hemorrhage, probably through down-regulation of Bax protein and up-regulation of Bcl-2 protein.