细胞外信号蛋白调节激酶5在异氟醚后处理减轻大鼠海马脑片缺氧无糖损伤中的作用  

Involvement of ERK5 in Isoflurane posttreatment-mediated protective effect on hippocampal oxygen-glucose deprivation injury in rats

作　　者：崔迪 王胜[1] 葛明月 王芹 殷姜文 代志刚[1] 司军强[2] 

机构地区：[1]石河子大学医学院第一附属医院麻醉科,新疆石河子832008 [2]石河子大学医学院生理教研室,新疆石河子832000

出　　处：《中国现代医学杂志》2017年第21期1-6,共6页China Journal of Modern Medicine

基　　金：国家自然科学基金(No:81360203)

摘　　要：目的探讨异氟醚后处理大鼠海马脑片缺氧无糖(OGD)损伤神经保护机制中细胞外信号蛋白调节激酶5(ERK5)的作用。方法使用雄性SD大鼠,将其麻醉后取出海马组织,制成离体脑片,然后随机进行正常对照组(Con组)、损伤组(OGD组)和药物处理组的处理。采用花粉活力染色(TTC)法评价各组脑片损伤程度,采用碘化丙啶(PI)染色法检测海马CA1区神经细胞凋亡程度,采用实时荧光定量聚合酶链反应(q RT-PCR)测定细胞外调节蛋白激酶信使核糖核酸(ERK5 m RNA)的表达,采用Western blot法检测ERK5蛋白的表达与磷酸化水平。结果与Con组比较,OGD组脑片损伤程度升高、海马CA1区凋亡细胞增多,海马组织内ERK5 m RNA和p-ERK5表达升高(P<0.05);XMD组阻断ERK5 m RNA和p-ERK5表达,脑片损伤程度升高、海马CA1区凋亡细胞增多(P<0.05)。与OGD、1.5%ISPOC和4.5%ISPOC组比较,3.0%ISPOC组脑片损伤程度减轻、海马CA1区凋亡细胞减少,海马组织内ER K5 m R N A和p-ER K5表达升高(P<0.05)。与3.0%ISPO C组比较,XMD阻断ISPOC海马组织内ERK5 m RNA和p-ERK5表达,脑片损伤程度升高、海马CA1区凋亡细胞增多(P<0.05)。结论一定浓度的异氟醚后处理大鼠海马脑片对抗O GD损伤的保护性机制可能与上调ER K5 m R N A和ERK5磷酸化水平有关。Objective To investigate the role of extracellular signal-regulated protein kinase 5（ERK5） on Isoflurane posttreatment-mediated decrease of hippocampal injury in rat models of oxygen-glucose deprivation（OGD）. Methods Male SD rats were randomly divided into four groups： the normal control（Con） group, the OGD group, the XMD group, and the ISPOC group. Rats were anesthetized followed by harvest of the hippocampus for further preparation of tissue slices. Histological analysis of hippocampus was achieved by 2%2, 3, 5-triphenyltetrazolium chloride（TTC） staining. Neuronal apoptosis in hippocampus CA1 region was analyzed by propidium iodide（PI） fluorescence staining. The expression level of ERK5 m RNA was determined by real-time fluorescent PCR. The ERK5 protein expression and phosphorylation were detected by Western blot. Results Compared with the Con group, the degree of hippocampal injury, apoptosis rate in hippocampal CA1 region and the expression levels of ERK5 m RNA and p-ERK5 in the OGD group were increased significantly（P〈0.05）. In the XMD group, the expression levels of ERK5 m RNA and p-ERK5 were decreased, and the degree of tissue injury and the apoptosis rate in hippocampal CA1 region increased（P〈0.05）. Compared with the group 3.0% ISPOC, XMD8-92 independently diminished the expression of ERK5 m RNA and phosphorylation of ERK5 in the hippocampus, and enhanced tissue injury as well as apoptosis rate in the XMD ＋ISPOC group（P〈0.05）. Conclusions The protective effect of Isoflurane posttreatment on hippocampal OGD injury in rats may be related to the upregulation of ERK5 m RNA and phosphorylation of ERK5.

关 键 词：麻醉药 异氟醚后处理 细胞外信号调节MAP激酶类 脑缺血 海马 

分 类 号：R332[医药卫生—人体生理学]