鼠急性全脑缺血再灌注后葛根素对海马CA1区Bcl-2、Bax表达的影响

目的　观察全脑缺血再灌注后葛根素对神经细胞凋亡相关基因Bcl 2、Bax表达的影响。方法　采用免疫组织化学法、原位末端标记法检测大鼠全脑缺血再灌注不同时间内海马CA1区Bcl 2和Bax蛋白表达水平及凋亡细胞数的变化。结果　①脑缺血再灌注后 ,海马CA1区Bcl 2蛋白的表达随再灌注时间不同而变化 ,缺血 10min后再灌注 6h达高峰 ;葛根素治疗组Bcl 2蛋白的表达于相应的时间点明显增加 ;②Bax蛋白表达在再灌注 2 4h达高峰 ,葛根素治疗组Bax蛋白表达在相应时间点则下降 ;③神经细胞凋亡数随再灌注时间延长而增加 ,葛根素可减少神经细胞凋亡数。结论　在全脑缺血再灌注后细胞凋亡中 ,Bcl 2、Bax发挥重要作用 ;葛根素通过上调Bcl 2蛋白的表达 ,下调Bax蛋白的表达抑制细胞凋亡发挥神经保护作用

Effects of puerarin on the expression of Bcl-2 and Bax in rat hippcampal CA1 after acute global cerebral ischemia and reperfusion

AIM To study the effects of puerarin on the expression of Bcl-2 and Bax, genes relating to neuronal apoptosis after cerebral ischemia and reperfusion. METHODS After global cerebral ischemia followed by reperfusion, changes in protein expression of Bcl-2 and Bax were detected by immunohistochemical method. The number of neuronal apoptosis was assessed by TUNEL. The effects of puerarin intervention were observed. RESULTS In CA1, the level of positive expression of Bcl-2 varied to the duration of reperfusion and the peak level was at 6 h reperfusion after 10 min global cerebral ischemia,the peak expression of Bax was at 24 h. The number of neuronal apoptosis after cerebral ischemia reperfusion was increased. In puerarin group, the expression of Bcl-2 was up-regulated and that of Bax was down-regulated, the number of neuronal apoptosis after cerebral ischemia reperfusion was decreased. CONCLUSION Our result indicate that Bcl-2 may restrain apoptosisl. Bax may promote apoptosis after cerebral ischemia and reperfusion and puerarin ameliorate ischemic damage by reducing the apoptosis through regulating Bcl-2 and Bax.