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目的探讨细胞外信号调节激酶1/2(extracellular signal-regulated kinase1/2,ERK1/2)在糖尿病脑缺血再灌注大鼠海马CA4区神经元表达的意义。方法在链脲佐菌素性糖尿病大鼠脑缺血再灌注模型基础中,应用TUNEL、免疫组化方法观察糖尿病脑缺血组与正常血糖脑缺血组在全脑缺血15min、再灌注1h海马CA4区神经元凋亡和磷酸化ERK1/2(P-ERK1/2)的表达变化。结果糖尿病脑缺血组在缺血15min、再灌注1h海马CA4区神经元凋亡发生率均明显高于正常血糖脑缺血组(P<0.05);糖尿病脑缺血组各时间点磷酸化ERK1/2明显增高,于再灌注1h明显高于正常血糖组(P<0.01)。结论糖尿病加重脑缺血再灌注神经元的损伤,其机制可能与ERK1/2的激活有关。
Objective To investigate the significance of extracellular signal-regulated kinase1 / 2 (ERK1 / 2) expression in neurons of hippocampal CA4 area in diabetic rat with cerebral ischemia / reperfusion. Methods In the model of focal cerebral ischemia-reperfusion in streptozotocin-induced diabetic rats, TUNEL and immunohistochemical methods were used to observe the changes of cerebral ischemia and normal blood glucose in cerebral ischemia 15min, reperfusion 1h Changes of neuronal apoptosis and phosphorylation of ERK1 / 2 (P-ERK1 / 2) in hippocampal CA4 region. Results The incidence of neuronal apoptosis in hippocampal CA4 area of ischemic cerebral ischemia group was significantly higher than that of normal cerebral ischemia group (P <0.05) at 15 min after ischemia, and phosphorylated ERK1 / 2 significantly increased at 1h after reperfusion was significantly higher than the normal glucose group (P <0.01). Conclusions Diabetes mellitus can aggravate the neuronal damage induced by cerebral ischemia and reperfusion. Its mechanism may be related to the activation of ERK1 / 2.