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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。
Objective To investigate the effects of blood glucose stabilization on neuronal apoptosis induced by cerebral ischemia in rats. Methods Normal SD rats were randomly divided into 4 groups: sham operation group (CON), global cerebral ischemia / reperfusion group (I / P), blood glucose level fluctuation group (BGF) and blood glucose level stabilization group The spatial resolution of the animals was observed. The phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1 / 2) was studied by Western blotting, and the terminal deoxynucleotidyl transferase mediated dUTP nick end labeling Apoptosis. Results The expression of phosphorylated ERK1 / 2 in hippocampus increased significantly at 3 h and 5 d after global cerebral ischemia / reperfusion in rats. The level of phosphorylated ERK1 / 2 in hippocampus maintained by insulin infusion could increase the level of ERK1 in hippocampus at ± 0.5 mmol / L preoperative level / 2 phosphorylation; however, there was no significant difference in the level of phosphorylation of ERK1 / 2 phosphorylation between ± 1.2mmol / L group and ischemia-reperfusion group. At 5 days after reperfusion, the water maze result was consistent with that of brain tissue. The apoptosis of brain tissue in stable blood glucose level was significantly relieved compared with ischemia group. The degree of phosphorylation of ERK1 / 2 was opposite to that of brain tissue. Conclusions Intraoperative maintenance of blood glucose may regulate neuronal apoptosis induced by ischemic brain injury through ERK1 / 2 signaling pathway.