GM_1对大鼠脑缺血再灌注后bcl-2、bax表达的影响

目的:探讨神经节苷脂GM_1对大鼠急性局灶性脑缺血再灌注损伤后凋亡相关基因bcl-2、bax表达的影响。方法:用线栓法制成大鼠大脑中动脉(MCA)闭塞及再通模型,利用免疫组化,观察一侧MCA缺血30分钟,再灌注5小时后病变侧海马CA1区bcl-2、bax表达的情况以及GM_1对其表达的影响。结果:假手术对照组海马区CAI可见bcl-2及少量bax表达。缺血/再灌注后,该区bcl-2及bax表达增加(分别P<0.01),且以bax表达明显占优势,bax染色阳性细胞以小体积,核固缩的凋亡细胞为主。应用GM_1后bcl-2表达进一步增加(P<0.01),而bax蛋白水平变化不明显,bcl-2与bax蛋白比值增加,bax染色阳性细胞胞体趋于正常,但核仍大而圆。结论:GM_1确实可以通过调节脑局灶性缺血/再灌注后bcl-2、bax表达而发挥神经保护作用。

The effect of GM1 on expression of bcl-2、bax in rat brain following acute focat cerebral ischemia and reperfusion

Objective: To approach the effect of ganglisoide GM1 on expression of bcl-2、bax genes in rat brain following a-cute focal cerebral ischemia and reperfusion. Methods The rat model of focal cerebral ischemia and reperfusion induced by string-embolic method. Using Immunohistochemistry method bcl-2 and bax protein positive cells were counted in three groups, namely, false operation group, ischemia-reperfusion group, and GM1 group (20mg/kg GM1 was injected into abdominal cavity after ischemia lasting 10 minutes). Results Bcl-2 and bax protein positive cells were increasing in rat brain following acute focal cerebral ischemia and reperfusion (P <0.01 respectively). The shapes and proportion of these two kinds of cells were significant different after the therapy of GM1(P <0.01) . Conclusion: This study indicates that ganglioside GM1 could obviously have the neuroprotective effect by regulating the expression of bcl-2、 bax genes in rat brain following acute focal cerebral ischemia and reperfucion.