环鸟苷酸依赖性蛋白激酶拮抗酒精性中枢神经细胞毒性机制研究  

Role of cGMP-dependent protein kinase against ethanol neurotoxicity of cerebellar granule cells

作　　者：戴德[1] 

机构地区：[1]广东医学院附属医院耳鼻咽喉科,湛江524001

出　　处：《第三军医大学学报》2006年第24期2434-2436,共3页Journal of Third Military Medical University

基　　金：湛江市科学技术局科研基金资助项目(2006C01021)~~

摘　　要：目的探讨环鸟苷酸依赖性蛋白激酶对酒精致鼠小脑颗粒细胞(cerebellargranulecells,CGC)毒性作用的影响机制。方法通过光学显微镜观察一氧化氮(NO)释放剂,环鸟苷酸及环鸟苷酸依赖性蛋白激酶抑制剂对鼠小脑颗粒细胞存活的影响。结果NO释放剂,环鸟苷酸在无酒精组中促进细胞的生存,并能对CGC产生保护作用,减少酒精对细胞的杀死。环鸟苷酸依赖性蛋白激酶抑制剂可抑制二者对细胞的作用。结论环鸟苷酸依赖性蛋白激酶在NO释放剂和环鸟苷酸促鼠小脑颗粒细胞的存活和抵抗酒精性神经毒性过程中具有重要的作用。Objective To analyze the function of cGMP-dependent protein kinase （PKG） in the survival of cultured rat cerebellar granule cells （CGC）. Methods CGC culture was incubated for 24 h before addition of ethanol and different reagents, such as Deta-NONOate （a NO donor） , Br-cGMP and Rp-8-pCPT-cGMPS （a cGMP-dependent protein kinase inhibitor）. After the treatment, samples were incubated for another 24 h, then the cells were collected and counted by using hemocytometer. Results Deta-NONOate and Br-cGMP enhanced the cell survival in the absence of ethanol, indicating their neurotrophic effects. They showed neuroprotective effect on the cultured CGC since they could reduce the ethanol-induced cell death. Inhibiting PKG with Rp-8-pCPT-cGMPS could eliminate both neurotrophic and neuroprotective effects mediated by Deta-NONOate and Br-cGMP. Conclusion cGMP-dependent protein kinase plays a key role in the cultured CGC survival and protects the cells against ethanol neurotoxicity.

关 键 词：小脑颗粒细胞 环鸟苷酸依赖性蛋白激酶 神经营养 神经保护 

分 类 号：R345.7[医药卫生—基础医学] R741.02