摘要
目的观察葛根素对局灶性脑缺血大鼠海马中促红细胞生成素(EPO)和信号转导与转录活化因子5(STAT-5)表达的影响,并探讨其可能的信号转导途径.方法采用线栓法制备大鼠大脑中动脉闭塞局灶性脑缺血模型,将SD大鼠随机分为模型干预组、模型对照组和假手术组,模型干预组及模型对照组根据干预时间不同又随机分为2 h组、12 h组、24 h组,用TTC染色和免疫组化染色观察大鼠脑梗死体积及海马CA3区EPO和STAT-5蛋白的表达水平。结果 (1)模型干预2 h组及12 h组的梗死体积明显小于模型对照组各对应时间点(P<0.05),而24 h组与模型对照组比较,梗死体积虽有所缩小但尚不具有明显差异;(2)各时间点模型对照组和模型干预组大鼠海马CA3区EPO和STAT-5的表达水平均较假手术组明显增高,但模型干预组EPO和STAT-5的表达水平均较模型对照组明显降低。结论局灶性脑缺血后应用葛根素治疗可以减小脑梗死体积,降低海马CA3区EPO和STAT-5阳性细胞数,且葛根素有可能是通过EPOR-JAK2-STAT5信号传导途径而对缺血性脑损伤发挥保护性作用。
Objective To observe the effects of puerarin on the expression of erythropoietin and STAT- 5 signal transducers and activators of transcriptions in the hippocampus of rats with cerebral ischemia and to investigate its possible mechanisms. Methods Focal cerebral ischemia model was set up with middle cerebral artery occlusion by intraluminal block in this study. 210 healthy male SD rats were divided into 3 groups ran- domly： model intervention group, model control group and sham-operation group. The model intervention group and model control group were further divided into 3 groups according to the intervention time：2 h, 12 h,24 h group. TTC dying and immunohistochemistry dying were performed to assess infarct volume and the expres- sions of EPO and STAT5 in CA3 region of hippocapous. Results （1）compared with model control group,the infarct volume in 2 h intervention group and 12 h intervention group obviously decreased （P〈0. 05）. The in- farct volume in 24 h intervention group slightly reduced,but no significance yet. （2）Both in model intervention group and model control group, the number of EPO and STAT-5 positive cells in hippocampal CA3 region were much more than that in sham-operation group; but the expressions of EPO and STAT-5 at each time point in model intervention group were distinctly less than that in model control group. Conclusions The treatment of puerarin within 12 h after focal cerebral ischemia can diminish infarct volume,cut down the expression of EPO and STAT-5 in himppocampal CA3. EPOR-JAK2-STAT5 signal transduction may play a protective role in the process of ischemic cerebral injury.
出处
《卒中与神经疾病》
2013年第3期137-140,共4页
Stroke and Nervous Diseases
