黄芪提取物对大鼠海马神经元迟发性死亡的影响

目的探讨黄芪提取物(Extractofastragalus,EA)对全脑缺血再灌注7d引起的大鼠海马神经元迟发性死亡的作用。方法用四动脉阻断法造模,观察背侧海马神经元的超微结构;CA1区神经元结构、正常神经元计数;免疫组化法检测胶质纤维酸性蛋白(GFAP)的表达。结果与缺血再灌(I/R)组比较,EA能改善背侧海马神经元超微结构;抑制CA1区正常神经元数目的减少,I/R组为38±11.5,EA(20、40mg·kg-1)分别为63±12.8(P<0.05)和77±16(P<0.01);降低GFAP的表达,I/R组GFAP阳性细胞数为69±10.7,EA三个剂量组分别为53±5.6(P<0.05)、39±7.1(P<0.01)、46±7.6(P<0.05)。结论EA能抑制全脑缺血再灌注7d大鼠海马迟发性神经元死亡,可能与其抑制海马CA1区星形胶质细胞(AS)过度增生有关。

Effects of extract of astragalus on hippocampal delayed neuronal death in rats

Aim To study the effects of extract of astragalus on hippocampal delayed neuronal death of totalcerebral ischemia and 7 days reperfusion in rats.Methods Global ischemia was made by four-vessel occlusion. Electron microscope was used to observe the ultramicrostructure of dorsal hippocampal neurons.Light microscope was used to survey the structure of hippocampal neurons and to count the number of normal neurons in CA1 sector. Glial fibrillary acidic protein(GFAP) was detected by immune histochemistry.Results Compared with ischemia and reperfusion group(I/R),EA improved the ultrastructure of hippocampal neurons, suppressed the decrease of normal neurons in CA1 and degraded the expression of GFAP .The number of normal neurons in I/R group was 38±11.5,and in EA(20,40 mg·kg -1) groups,63±12.8(P<0.05)and 77±16(P<0.01)respectively. The number of GFAP positive cells in I/R group was 69±10.7, and in EA(20,40,80 mg·kg -1)groups,53±5.6(P<0.05),39±7.1(P<0.01)and 46±7.6(P<0.05)respectively. Conclusion EA can restrain hippocampal delayed neuron death of global ischemia and 7 d reperfusion in rats. It may suppress hyperplasy of astrocytes (AS) in hippocampal CA1 sector.