头孢曲松钠对大鼠蛛网膜下腔出血后认知功能的影响

目的 探讨头孢曲松钠（CEF）对大鼠蛛网膜下腔出血（SAH）后的认知功能的影响及其机制。方法 将68只成年SD大鼠随机分为4组:正常组（n=12）、对照组（n=24）、CEF低剂量治疗组（n=8）和CEF高剂量治疗组（n=24）。采用枕大池双次注血方法建立大鼠SAH模型。SAH后3 h经小脑延髓池缓慢注射100 μl CEF（高剂量组浓度为100 μmol/L，低剂量组浓度为50 μmol/L），对照治疗组注射等体积生理盐水。采用Morris水迷宫检测各组动物学习记忆能力；Western blot检测各组大鼠海马 Caspase-3和兴奋性氨基酸转运体2（EAAT2）的表达水平。结果 与对照组相比，CEF治疗组SAH后动物的水迷宫实验中的逃逸时间显著减少（P<0.05），大鼠海马组织中EAAT2的表达增加（P<0.05），Caspase-3的表达减少（P<0.05）。结论 CEF对SAH后具有显著的神经保护作用，CEF治疗可能通过上调星形胶质细胞EAAT2的表达逆转SAH诱导的神经损伤。

Effect of ceftriaxone on cognitive function after subarachnoid hemorrhage in the adult rats

Objective To explore the effect of ceftriaxone (CEF) on cognitive function after subarachnoid hemorrhage (SAH) and its mechanism in rats. Methods Sixty-eight adult rates were randomly divided into 3 groups i.e. CEF treatment group (n=32), control group (n=24) and normal group (n=12). The model of SAH was established by two injections of autogeneic blood into the cerebellar cisterna magna in the rats of the treatment and control groups. Thirty-two rats in the treatment group were divided into two subgroups, i.e. low dose subgroup (n=8) in which 50 μl CEF at concentration of 50μmol/L was injected into the cerebellar cisterna magna 3 hours after SAH and high dose subgroup (n=24) in which 100 μl CEF at concentration of 100 μmol/L was injected into the cerebellar cistern magna 3 hours after SAH. The functions of learning and memory were by Morris water maze test in all the groups 5 days after SAH. The levels of EAAT2 and Cleaved Caspase-3 expressions in the hippocampal tissues by Western Blot in all the groups 6, 12, 24 and 48 hours after SAH. Results The escape latent period was significantly shorter in the high-dose group than that in the control group (P<0.01). The level of EAAT2 expression was significantly higher, and the level of cleaved Caspase-3 expression was significantly lower in the hippocampal tissues in the high dose group than those in the control group 48 hours after SAH (P<0.05). Conclusion It is suggested that CEF has neuroprotective effect after SAH by the upregulation of EAAT2 expression in the hippocampal tissues in the rats.