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目的:探讨孤啡肽及其受体在创伤大鼠的神经免疫调节作用.方法:采用免疫组织化学,原位杂交,及细胞因子的生物活性检测技术,定量分析内源性孤啡肽及其受体在中枢神经系统的表达及腹腔巨噬细胞分泌IL-1及TNF-α的能力.结果:在正常条件下,孤啡肽及孤啡肽受体mRNA免疫阳性细胞广泛分布于皮层、海马及下丘脑.而在创伤应激作用下,阳性细胞数明显减少.而另一方面,腹腔巨噬细胞分泌IL-1及TNF-α的能力却明显增强.将对照组的~3H掺入值及吸光度定为100％,则在创伤应激作用下,二者的活性分别增强至233％及521％(1:4),195％及566％(1:8),233％及757％(1:16),214％及622％(1:32).侧脑室注射三种剂量的孤啡肽(0.55nmol,0.55nmol,2.75nmol)对IL-1及TNF-α的活性均有显著的下调作用.而且孤啡肽(0.55nmol)的作用能被其受体拮抗剂所阻断.结论:孤啡肽及其受体,作为新的内阿片肽系统,参与创伤应激介导的免疫调节.
Objective: To investigate the neuroimmunologic regulation of orphanin and its receptor in traumatic rats.Methods: The immunohistochemistry, in situ hybridization and bioassay of cytokines were used to quantitatively analyze the expression of orphanin and its receptor Receptor expression in the central nervous system and secretion of IL-1 and TNF-α by peritoneal macrophages.Results: Under normal conditions, immunopositive cells of orphanin and orphanin peptide receptor mRNA were widely distributed in the cortex, hippocampus And hypothalamus, while in traumatic stress, the number of positive cells decreased significantly.On the other hand, the ability of peritoneal macrophages to secrete IL-1 and TNF-α was significantly increased.Contrast the ~ 3H incorporation of the control group And absorbance at 100%, the activities of the two increased to 233% and 521% (1: 4), 195% and 566% (1: 8), 233% and 757% 1:16), 214%, and 622% (1:32) .Intraventricular injection of three doses of orphanin (0.55nmol, 0.55nmol, 2.75nmol) on IL-1 and TNF-α activity were significant Downregulation.And the role of orphanin (0.55nmol) can be blocked by its receptor antagonist.Conclusion: Orphanin and its receptor, as a new endogenous opioid peptide system, involved in trauma should Mediated immune regulation.