缺血早期Genistein对海马CA1区神经元保护作用机制的研究

目的 探讨缺血早期Genistein对脑缺血/再灌注后大鼠海马CA1区神经元的保护作用及其可能的机制.方法 采用四动脉结扎建立大鼠全脑缺血模型.实验动物随机分为假手术组、缺血/再灌注组、溶剂对照组、Genistein处理组.缺血5 min时,溶剂对照组、Genistein处理组分别尾静脉注射二甲基亚砜（l ml/kg）和Genistein（1 mg/kg）.Western blot和免疫荧光法检测大鼠海马CA1区HAX-1蛋白的表达,焦油紫染色法观察海马CA1区神经元的存活情况.结果 与对照组比较,Genistein处理组在再灌注3h时HAX-1蛋白表达水平显著升高（P＜0.05）,免疫荧光实验结果与此一致.焦油紫染色结果显示,Genistein处理组与对照组相比较,海马CA1区存活的神经元细胞明显增加（P＜0.05）.结论 缺血早期Genistein对脑缺血造成的神经元损伤有明显的保护作用,这一作用可能是通过增加HAX-1蛋白表达水平来实现的.

Protective effects of genistein on early ischemia in hippocampal CA1 neurons

Objective To explore the protective effects of genistein on ischemia/reperfusion injury in hippocampal CA1 neurons and its underlying mechanism. Methods The fourvessel occlusion method was used to establish a rat model of global cerebral ischemia. Animals were randomly divided into four groups ： a sham operation group, an ischemia/reperfusion group, a solvent - exposed group, and a genistein treatment group. Five minutes after ischemia, DMSO and genistein （ both 1 mg/kg） were injected via the tail vein into the solvent - exposed and genistein groups respectively. The expression of HAX - 1 protein in the CA1 region of the hippocampus was assessed by western blotting and immunofluorescence. The survival rats of hippocampal CA1 neurons were assessed by the cresyl violet staining. Results Compared with the solvent - exposed group, the protein level of HAX - 1 was significantly increased 3 hours after reperfusion in the genistein treatment group （ P 〈 0.05 ）, which was consistent with immunofluoreseence results. After the cristal violet staining, genistein treatment could remarkably enhanced the survival rates of hippocampal CA1 neurons than the control （P 〈 0.05）. Conclusion Genistein can protect neurons from ischemia injury at early stage, which may be achieved by up - regulating the protein level of Hax - 1.