黄芪对脑缺血再灌注后神经细胞凋亡的影响及机制研究

Study of Radix Astragali on Neuronal Apoptosis in Reperfused Local Cerebral Ischemia Rats Brains

目的研究黄芪对脑缺血再灌注大鼠脑神经细胞凋亡的影响,并通过对皮质及纹状体缺血周围区PI3-K和Akt的检测进一步探讨黄芪减少神经细胞凋亡的分子机制。方法采用ZeaLonga线栓法制备大鼠大脑中动脉闭塞(MCAO)模型,缺血3h后再灌注。分为假手术组、模型组、胞磷胆碱组、黄芪组。术后分12、24、48h3个时间点作神经功能评分;TUNEL法观察凋亡的情况;免疫组化法观察皮质及纹状体缺血周围区PI3-K和Akt表达强度。结果神经功能评分显示黄芪组和胞磷胆碱组恢复明显优于模型组,黄芪组和胞磷胆碱组相近;黄芪组凋亡阳性细胞数均少于模型组及胞磷胆碱组;模型组PI3-K和Akt免疫阳性细胞平均数显著低于黄芪组和胞磷胆碱组。于再灌注48h黄芪组与胞磷胆碱组间差异显著。结论黄芪可减轻大鼠脑缺血再灌注后神经细胞凋亡,能刺激PI3-K/Akt信号通路的表达。

Objective： To study the therapeutic effects of radix astragali injection （RA） on phosphatidyrlinositol 3 - kinase （PI3 - K）, serine threonine kinase （Akt） and apoptosis in rats brains following local cerebral ischemia reperfusion. Methods： Nighty male adult SD rats were randomly divided into four groups： the sham - operated group, the model group, the citicoline group and the RA group. The model of middle cerebra/artery occlusion（MCAO） was established by thread ligation method. Neurological system symptoms were evaluated after 12, 24, 48h of ischemia reperfusion. Then the rats were decapitated and rats brains were taken for histopathological, TUNEL and immunohistochemistry examinations. Positive reacted cells of apoptosis, PI3 - K and Akt were counted under light microscope at different time points of ischemia reperfusion. Results：RA injection could significantly alleviate neurological system damage symp - toms and apoptosis. Histopathological examination showd that the cerebral ischemie damage in the RA group was significantly milder than that in the model group. As compared with the model group, positive reacted cell amounts of apoptosis were greatly declined in RA group and citieoline group. Positive immune reacted cell amounts of PI3 - K and Akt were greatly enhanced in RA group as compared with the mode/group and the citicoline group in 48h ischemia reperfusion. Conclusions： The protective effects of the RA injection therapy against cerebral ischemia reperfusion injury might be associated with improving the positive expressions of PI3 - K and Akt.