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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 -NOS通路的过程
Objective To explore the mechanism of κ opioid receptor after spinal cord injury induced by dynorphin (Dyn). Methods The experiment was divided into isotonic saline control group, DynA (1- 17) injuried group and nor-BNI specific antagonist of nor-BNI treatment group, 5-methyldihydrodibenzopyrimidine (3H-MK80 1) binding assay was used to determine the function of N-methyl-D-aspartate (NMDA) receptor in the ventral spinal cord and the ventral Spinal cord native and inducible nitric oxide synthase (cNOS, iNOS) activity, and immunohistochemistry was used to observe the neuronal cNOS (ncNOS) immunocompetence. Results Injection of 3 mmol Lnor-BNI significantly inhibited dysfunction and pathological damage induced by DynA (1- 17) and significantly antagonized the effect of DynA (1- 17) injection 10 min before subarachnoid injection of 2 mmol LDynA (1- 17) Induced 3H-MK80 1 binding, increased cNOS and iNOS activity, and significantly inhibited the expression of ncNOS immunoreactivity induced by DynA (1- 17). Conclusion During the process of spinal cord injury induced by Dyn, κ opioid receptor is involved in the up-regulation of NMDA receptor-NOS pathway in ventral spinal cord by Dyn