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

在雄性大鼠中，通过心脏骤停和复苏（CAR）5分钟诱导全脑缺血，并给予或不给予急性葡萄糖（2g/kg i. p.）。CAR后两周，提取脑并制备脑切片。在两组的海马CA 1区均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（receptor for advanced glycation end products）表达，葡萄糖给药组和赋形剂给药组，但在两组之间未检测到统计学显著性差异。两组的神经功能缺损评分（可以检测大脑功能损伤）相似。我认为原因是由于样本量不够或CAR单独引起高血糖。

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.