强啡肽致脊髓损伤后κ阿片受体机制的新证据  

Effects of kappa-opioid receptor on dynorphin-induced spinal cord injury

作　　者：胡文辉[1] 刘娜[2] 李芳[1] 强文安 廖维宏[1] 任民峰[2] 

机构地区：[1]第三军医大学附属大坪医院野战外科研究所,重庆400042 [2]中国医学科学院基础医学研究所

出　　处：《中华创伤杂志》2000年第5期286-288,共3页Chinese Journal of Trauma

基　　金：国家自然科学基金资助项目!(39370786)

摘　　要：目的　进一步探讨强啡肽 (Dyn)致脊髓损伤后κ阿片受体机制。　方法　实验分为等渗盐水对照组、DynA(1- 17)致伤组和特异性κ阿片受体拮抗剂nor-BNI治疗组 ,采用 5 -甲基二氢二苯并环庚稀亚氨马来酸 (3H -MK80 1)结合实验测定腹侧脊髓N -甲基 -D -天门冬氨酸(NMDA)受体功能 ,3H -左旋精氨酸 (3H -L -Arg)转化法测定腹侧脊髓原生型和诱导型一氧化氮合酶 (cNOS、iNOS)活性 ,并采用免疫组化技术观测神经元性cNOS(ncNOS)免疫活性。　结果　在蛛网膜下腔注射 2mmol LDynA(1- 17) 10 μl之前 10min ,注射 3mmol Lnor-BNI可显著对抗DynA(1- 17)引起的功能障碍和病理损害 ,并明显对抗DynA(1- 17)引起的3H -MK80 1结合升高及cNOS和iNOS活性增强 ,也明显对抗DynA(1- 17)诱导的脊髓腹角细胞ncNOS免疫活性表达。　结论　Dyn致脊髓损伤过程中 ,κ阿片受体参与Dyn上调腹侧脊髓NMDA受体Objective [WT5”BZ]To provide new evidences for the κ-opioid receptor mechanism in dynorphin(Dyn)-induced spinal cord injury. Methods The functional activity of N-methyl-D-aspartate (NMDA) receptor and the activity of constitutive and inducible nitric oxide synthase(cNOS and iNOS) were measured respectively with 3 H-MK801 binding and 3 H-L-arginine conversion in the ventral spinal cord of rats after Dyn A(1-17) treatment and selective κ-opioid receptor antagonist nor-BNI pretreatment. Results Pretreatment with nor-BNI (3 mmol/L) 10 min before subarachnoid injection of Dyn A(1-17) (2 mmol/L) could significantly antagonize Dyn-induced permanent paraplegia and increase 3 H-MK801 binding as well as cNOS and iNOS activities in the ventral spinal cord. Nor-BNI also apparently attenuated Dyn-induced increases in immunoreactivities of neuronal cNOS. Conclusions κ-opioid receptor might be involved in the enhancement of the function of NMDA-NOS/NO pathway after Dyn-induced spinal cord injury

关 键 词：强啡肽 脊髓损伤 阿片样受体 一氧化氮 

分 类 号：R971[医药卫生—药品]