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目的 :研究糖皮质激素治疗癫的机制及其与白细胞介素 2受体 (IL 2R)的关系。方法 :用腹腔注射美解眠制作大鼠癫模型 ,致前后分组分别给予地塞米松 ,观察大鼠出现癫发作的潜伏期及持续时间 ,并用脑电图仪和免疫细胞化学方法研究地塞米松对癫大鼠脑电图和皮层及海马区IL 2Rβ免疫反应阳性细胞的影响。 结果 :对照组无癫发作。致前给予地塞米松组大鼠较癫组大鼠癫发作潜伏期延长 (12 .2 5± 1.6 3对 3.85± 0 .81min) ,持续时间缩短 (9.6 8± 3.16对 14 .98±2 .18min) (P <0 .0 1) ,脑电图高电位样波发放减少 ,顶区皮层和海马IL 2Rβ免疫反应阳性细胞数减少 (5 .31± 1.11对 12 .84± 1.5 3,2 .80± 0 .76对 6 .79± 1.14个 ) (P <0 .0 1)。致后给予地塞米松组 ,上述指标与癫组相比 ,差异无显著意义 (13.86± 2 .31对 12 .84± 1.5 3,5 .89± 0 .95对 6 .79± 1.14个 )(P >0 .0 5 )。结论 :糖皮质激素抑制癫发作与其快速膜效应及通过IL 2对免疫 神经 内分泌网络的调节有关。
Objective: To study the mechanism of glucocorticoid treatment of epilepsy and its relationship with interleukin 2 receptor (IL 2R). Methods: The model of epilepsy was induced by intraperitoneal injection of Mi-Jian-Mian. Dexamethasone was given to the rats before and after treatment. The latency and duration of epileptic seizures in rats were observed. EEG and immunocytochemistry Effects of dexamethasone on EEG and IL 2Rβ immunoreactive cells in cortex and hippocampus of epileptic rats. Results: The control group had no epileptic seizures. In the dexamethasone group, the latent period of epileptic seizures in rats in the epilepsy group was longer than that in the epilepsy group (12.25 ± 1.6 3 vs 3.85 ± 0.81min), and the duration was shorter (9.6 8 ± 3.16 vs 14.98 ± (P <0.01), P <0.01, P <0.01), the EEG sample release decreased, and the number of IL 2Rβ immunoreactive cells in the apical cortex and hippocampus decreased (5.31 ± 1.11 vs 12.84 ± 1.53 , 2.80 ± 0.76 vs. 6.779 ± 1.14) (P <0.01). After dexamethasone group was induced by dexamethasone, there was no significant difference between the above indexes and epilepsy group (13.86 ± 2.31 vs 12.84 ± 1.5, 3.5.89 ± 0.95 vs. 6.79 ± 1.14 ) (P> 0 .0 5). CONCLUSIONS: Glucocorticoid-induced epileptic seizures are associated with its rapid membrane effect and regulation of the immune neuroendocrine network by IL-2.