兔脊髓空洞前状态蛋白激酶C对水通道蛋白4表达的调控作用  

Changes of PKC activity and its regulation on AQP4 expression in experimential presyrinx state in rab-bits

作　　者：孙国柱[1] 张庆俊[2] 王浩[1] 张更申[1] 

机构地区：[1]河北医科大学第二医院神经外科,石家庄050000 [2]北京大学人民医院神经外科

出　　处：《中华实验外科杂志》2006年第4期613-614,共2页Chinese Journal of Experimental Surgery

基　　金：河北省科技厅资助项目(002761100)

摘　　要：目的探讨PKC在脊髓空洞前状态中活性变化及其对AQP4调控作用。方法用新西兰兔56只制作模型,术后1、3、7、14、21d用免疫组织化学技术检测AQP4表达变化、应用底物磷酸化法测定胞膜、胞浆PKC活性。结果 Kaolin组动物AQP4于术后3 d开始减弱(IA 320．5± 44．2),7-14 d达到最低水平(IA 258．7±26．5),到21 d时有所回升(IA 321．5±46．1);胞膜PKC 活性术后1 d出现增加每分钟(5.67±0．26)pmol／mg,7-14 d达到最高水平每分钟(13．27±3．15 pmol／mg),21 d开始回落每分钟(8．85±1．56)pmol／mg,胞浆的PKC活性则呈相反趋势。结论脊髓空洞前状态形成中出现PKC移位激活,对AQP4进行磷酸化,参与了缺血、缺氧性脊髓水肿的形成。Objective To investigate the changes of PKC activity and its regulation on AQP4 expression during development of presyrinx state in rabbits. Methods The experimental models were established in 56 rabbits by intracisternal injection of Kaolin. The expression of AQP4 and PKC activity were measared with immunohisto-chemistry and substrate phosphorolysis kinase assay in 1, 3, 7, 14, 21d after determined. Results Comparing with control group, AQP4 expression was decreased on the 3rd day after operation （IA 320.5 ± 44.2）, reached its peak at 7th day, lasted to 14th day （IA 258.7 ± 26.5）, and recoved partially at 21st day （ IA 321.5 ± 46.1） in Kaolin group. Membrane PKC activity was increased from 1^st day （5.67 ± 0.26 pmol· mg^-1· min^-1）, reached its peak at 7^th day, lasted to 14th day （13.27　±3.15） pmol·mg^-1·min ^-1, and then began to drop （8.85　± 1.56） pmol·mg^-1·min^-1 in Kaolin group. Kytoplasm PKC activity showed an opposite tendency. Conclusion In experimental presyrinx state, translocational activation of PKC imposes phosphorylation on AQP4, involving in spinal edema from ischemia.

关 键 词：水通道蛋白4 脊髓空洞前状态 PKC 免疫组织化学 

分 类 号：R744.4[医药卫生—神经病学与精神病学] R-332[医药卫生—临床医学]