血糖稳定对大鼠脑缺血后海马神经元凋亡的影响

目的探讨血糖稳定对大鼠脑缺血所致的神经元凋亡的影响。方法将正常SD大鼠随机分为4组,假手术组(CON),全脑缺血再灌注组(I/P),血糖水平波动组(BGF)和血糖水平稳定组(BGS),水迷宫观察动物空间分辨力,使用免疫印迹技术对比研究细胞外信号调节激酶1/2(ERK1/2)的磷酸化,同时采用末端脱氧核苷酸转移酶介导的dUTP原位切口末端标记方法观察神经细胞凋亡。结果大鼠全脑缺血再灌注后3h和5d时海马区磷酸化ERK1/2表达明显增加;胰岛素控制输注维持血糖变动水平在术前水平的±0.5mmol/L组时可进一步增加海马ERK1/2磷酸化;但血糖变动水平在±1.2mmol/L组ERK1/2磷酸化表达与缺血再灌注组没有明显差异。再灌注5d时大鼠水迷宫结果与脑组织凋亡一致,血糖水平稳定组脑组织凋亡较缺血组明显减轻,磷酸化ERK1/2的程度与脑组织凋亡结果相反。结论术中维持血糖稳定可能通过ERK1/2信号通路调节大鼠缺血性脑损伤所致的神经元凋亡。

Role of glucostasis in Neuronal apoptosis of rat hippocampus after transient global brain ischemia

Objective To observe the role of glucostasis in Neuurconal apoptosis of rat hippoeampus after tramient global ischemia. Methods Normal SD rats randcxnized 4 groups, pseudcoperation group（CON）, global brain ischemia/ reperfusion group（I/P）, blood glucose fluctuation group（BGF） and blood glucose stabliliation group（BGS）. Morris water maze, immunoblot assay and TUNEL immunostaining were used to observe animal spatial resolution, p- ERK expressional level and neuronal apoptosis, respectively. Results expressional levels of p-ERK in hippocampus rise at 3 hour and 5 day after transient global ischemia, blood glucose stabilize at -＋ 0.5mmol/L range about preoperative level can further increase p- ERK hvels, while blood glucose fluctuate at ＋ 1.2mmol/L range about preoperative level has no significant difference compare to ischemia/reperfusion group. Result of Morris water maze is consistent with neural apoptosis, blcod glucose stabliliation can alleviate neural apoptosis after ischemia/reperfusion, p- ERK1/2 expressional level are converse with neural apoptosis. Conclusion perioperative glucostasis may regulate neuronal apoptosis of rat hippocampus after transient global brain ischemia through ERK1/2 signal pathway.