ERK1/2的激活参与七氟醚预处理对大鼠海马脑片缺氧无糖损伤的保护作用  

The activation of ERK1/2 participates in neuroprotection induced by sevoflurane preconditioning on oxygen-glucose deprivation injury in rat hippocampal slices

作　　者：王志萍[1] 张永华[2] 夏鹏[2] 江山[2] 曾因明[2] 

机构地区：[1]徐州医学院附属医院麻醉科 [2]江苏省麻醉医学研究所

出　　处：《中国药理学通报》2007年第10期1367-1370,共4页Chinese Pharmacological Bulletin

基　　金：江苏省自然科学基金资助项目(NoBK2002138);江苏省教育厅资助项目(05KJB320139)

摘　　要：目的观察ERK1/2的激活在七氟醚预处理对大鼠海马脑片缺氧无糖损伤保护中的作用。方法采用脑片灌流及电生理技术,细胞外记录海马CA1区的顺向群锋电位(OPS);利用2,3,5-三苯基氯化四氮唑(TTC)染色定量比色方法分析脑片损伤程度。结果用4%七氟醚预处理海马脑片,可延迟OPS的消失时间,提高复氧后OPS的恢复程度和恢复率。以ERK1/2特异性抑制剂PD98059(50μmol.L-1)预处理海马脑片,可以取消七氟醚的作用。单独使用PD98059对OPS无明显影响。七氟醚预处理组组织损伤百分率明显低于其它各组。结论ERK1/2的激活参与了七氟醚预处理对大鼠海马脑片缺氧无糖损伤的保护作用。Aim To examine whether the activation of ERK1/2 is involved in neuroprotection of sevoflurane preconditioning on oxygen-glucose deprivation （OGD） injury in rat hippocampal slices. Methods By using electrophysiological technique, the amplitude of orthodromic population spike （OPS） in the stratum pyramidale of the CA1 region was measured. TYC staining was used to calculate the percentage of tissue injury. Results Pretreatment of the slices with 4% sevoflu- rane delayed the onset of OPS disappearance and improved the recovery of OPS after re-oxygenation. Pretreatment with ERK1/2 inhibitor PD98059 abrogated the effects induced by sevoflurane, while treatment of PD98059 alone had no effect on OPS. The percentage of tissue injury of sevoflurane group was significantly lower than that of other groups. Conclusion The activation of ERK1/2 participates in neuroprotection induced by sevoflurane preconditioning on oxygen-glucose deprivation injury in rat hippocampal slices.

关 键 词：ERK1/2 七氟醚 海马脑片 缺氧无糖损伤 

分 类 号：R-332[医药卫生] R322.81