葛根素对脑缺血再灌注后核因子kappaB表达的影响

目的：研究大鼠局灶性脑缺血再灌注后核因子kappaB(NF-κB)在时间和空间上表达的变化过程及葛根素对其的影响；方法：线栓法建立右侧大脑中动脉闭塞大鼠模型,分别于缺血90 min后再灌注2,6,12,24,72 h,缺血前1 h及随后每间隔6 h腹腔内给药。大鼠在各时间点断头取脑,测算脑梗死体积,免疫组织化学方法和免疫印迹法检测脑组织内NF-κB的表达。结果：大鼠缺血再灌注后,免疫组化分析提示NF-κB从细胞浆向细胞内移位,核内表达水平在6 h开始明显升高,在24 h达到高峰,72 h下降,其脑梗死体积随着再灌注时间延长而增加。葛根素明显降低NF-κB在缺血再灌注后24,72 h的表达及减小脑梗死体积。结论：脑缺血再灌注后,脑梗死周边区域出现NF-κB从胞浆至胞核的转位并伴表达增加,葛根素可能通过抑制NF-κB的表达,减轻缺血再灌注损伤。

Effects of puerarin on expression of nuclear factor kappaB after cerebral ischemia/reperfusion in rats

OBJECTIVE: To investigate the activation of nuclear factor kappaB (NF-KB) and the influence of puerarin on it after cerebral ischemia-reperfusion in rats. METHOD: Cerebral ischemia-reperfusion injury was induced by 90 min of middle cerebral artery (MCA) occlusion and followed by 2, 6, 12, 24, 72 h reperfusion. Puerarin or saline was intra-peritoneally injected 1h before MCA occlusion and then the drugs were administered once every six hours. The infarct volume and brain edema were determined by TTC stain. Level of NF-kappaB P65 subunit was determined by immunohistochemistry and western blot. RESULT: Immunohistochemistry revealed the translocation of NF-kappaB. A time course of NF-kappaB induction in brain showed that NF-kappaB P65 subunit obviously increased at 6 h, peaked at 24 h and then decreased by 72 h post-reperfusion. Puerarin decreased the level of NF-kappaB at 24, 72 h after reperfusion. There was a decrease trend in brain infarct volume between puerarin and control. CONCLUSION: NF-kappaB is translocated and its level is increased after ischemia-reperfusion. Puerarin may attenuate the ischemia-reperfusion injury through inhibition of NF-kappaB activation.