Involvement of receptor for advanced glycation end products for hyperglycemia-induced aggravation of white matter damage by cerebral ischemia

用心脏停搏复苏(CAR)5min复制雄性大鼠全脑缺血模型，分别给予或不给予急性葡萄糖(2g/kg，ip)。在开车两周后，提取了大脑，并准备了脑片。给糖组和给药组在海马CA1区均可检测到小胶质细胞活化、神经元和轴突损伤以及晚期糖基化终产物受体(RAGE)的表达，但两组间差异无统计学意义。可以检测大脑功能损害的神经功能缺陷评分在两组中是相似的。我认为原因是样本量不够，或者是汽车本身导致了相当高的血糖。

Global cerebral ischemia was induced by 5 min of cardiac arrest and resuscitation (CAR) in male rats with or without acute glucose administration (2g/kg i.p.). Two weeks after the CAR, the brain was extracted and brain slices were prepared. Microglial activation, neuronal and axonal injuries, and RAGE (receptor for advanced glycation end products) expression were detected in the hippocampal CA1 region in both groups, i.e., a glucose-administered group and a vehicle-administered group, but the statistically significant differences of those were not detected between the two groups. Neurologic deficit scores, which can detect functional damage in the brain, were similar in the both groups. I assume that the reason is due to the fact that sample size was not enough or that CAR alone caused rather hyperglycemia.