缺氧缺血性脑损伤新生大鼠海马突触体素的表达及当归调控作用

目的探讨脑缺氧缺血对新生大鼠海马齿状回突触体素表达的影响及当归注射对其表达的调控作用。方法取7日龄健康SD新生大鼠33只,随机分为对照组、缺氧组和当归组各11只。缺氧组和当归组新生大鼠在无菌环境下结扎左侧颈总动脉,术后护理2 h后置于三气培养箱持续缺氧2 h,制作新生鼠缺氧缺血性脑损伤（HIBD）模型,对照组仅行假手术,不结扎左侧颈总动脉、不缺氧。术后第8 d开始,缺氧组和对照组大鼠经腹腔注射生理盐水（8ml/kg）,连续7 d;当归组用等量当归注射液（250 g/L）代替生理盐水。于生后第22 d取大鼠脑组织,常规石蜡包埋、经海马切片,行突触体素（SY）免疫组化染色,图像分析海马齿状回SY阳性细胞的积分光密度（IOD）值。结果缺氧组大鼠海马齿状回SY阳性细胞的IOD值较对照组降低,而当归组SY阳性细胞的IOD值较缺氧组增高。结论脑缺氧缺血可降低新生大鼠海马齿状回SY的表达,而当归注射液对缺氧缺血性脑损伤新生大鼠可能具有保护作用。

The Synaptonphysin Expression in Hippocampal of the Hypoxic-Ischemic Brain Damaged Neonatal Rat and the Regulatory Effect of Angelica Sinensis

Objective To explore the expression of synaptophysin（SY） in hippocampal dentate gyrus neurons of the neonatal rats induced by hypoxic-ischemic brain damage（HIBD）,and to study the regulatory effect of Angelica sinensis injection on SY expression.Methods The seven-day-old healthy Sprague Dawley rats（n=33） were divided into three groups,namely control group（CG,n=11）,hypoxia group（HG,n=11）,and Angelica group（AG,n=11）.The left carotid artery of HG and AG rats were ligated and placed into the three-gas incubator for two hours to make the HIBD model of neonatal rats,CG only was received a Sham-operation without carotid artery ligation.Following the eight day operation,HG and CG were received intraperitoneal normal saline injection（8 ml/kg） for 7 days.And AG was made the same as HG during procedures,but injected Angelica sinensis instead of normal saline injection.The neonatal rats of each group were fed for 22 days.The 22-day-old juvenile rats,brain tissue of juvenile rats were taken,paraffin-embedded and sectioned through hippocampal.The expression of SY was detected with immunohistochemistry technology and the IOD of SY positive cells in hippocampal dentate gyrus neurons was analyzed.Results The IOD value of the SY positive cells in HG was lower than that of CG,while the IOD value of SY positive cells was higher than that of HG.Conclusion Angelica sinensis injection may play a protective role in the expression of synaptophysin during inhibition on hippocampal dentate gyrus neurons induced by HIBD.