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目的探讨白细胞介素2(IL-2)致痫与NMDA受体(NMDAR)和雌激素受体(ER)的关系。方法应用免疫组织化学、免疫荧光双标和激光共焦显微镜技术研究IL-2致痫大鼠及经免疫抑制剂预处理后再致痫大鼠脑内NMDAR-1、ER的表达变化以及NMDAR/ER和NMDAR/IL-2R共存情况。结果大鼠侧脑室注射IL-2以后,动物出现明显的癫痫发作,其大脑皮质和海马部位NMDAR-1及ER表达较对照组明显增多,免疫反应平均吸光度(A)值与对照组相比有极显著性差异;而用IL-2抑制剂环胞霉素(CsA)或糖皮质激素(G)预处理后再注射IL-2,动物未出现或仅出现轻微的癫痫发作,其NMDAR-1和ER表达较IL-2组明显减少(P<0.05)。研究还观察到大鼠脑内大脑皮质和海马部位NMDAR/ER或NMDAR/IL-2R之间存在着广泛共存。结论IL-2有致痫作用,NMDAR-1I、L-2R和ER在致痫活动中可能存在协同和互动作用。
Objective To investigate the relationship between interleukin 2 (IL-2) -deletion and NMDA receptor (NMDAR) and estrogen receptor (ER). Methods The expression of NMDAR-1 and ER in brain of IL-2-induced epileptogenic rats and immunosuppressive agents pre-treated with immunofluorescence double labeling and confocal laser scanning microscopy was used to detect the expression of NMDAR-1, ER in NMDAR / Coexistence of ER and NMDAR / IL-2R. Results After IL-2 injection into the lateral ventricle, the animals showed obvious seizures. The NMDAR-1 and ER expressions in the cerebral cortex and hippocampus were significantly increased compared with those in the control group. The mean value of immunoreactivity (A) (P <0.05). However, IL-2 was pretreated with cyclosporine (CsA) or glucocorticoid (G), and the animals showed no or only mild seizures. NMDAR-1 And ER expression was significantly decreased compared with IL-2 group (P <0.05). The study also observed widespread coexistence of NMDAR / ER or NMDAR / IL-2R in the cerebral cortex and hippocampus in rat brains. Conclusion IL-2 can induce epilepsy. There may be synergistic and interactive effects of NMDAR-1I, L-2R and ER in epileptic activity.