地塞米松对TNF-α致痫大鼠海马GABAA受体表达的影响

EFFECTS OF DEXAMETHASONE ON THE EXPRESSION OF GABA A RECEPTOR IMMUNOREACTIVE CELLS IN HIPPOCAMPUS OF SEIZURES RATS INDUCED BY TUMOR NECROSIS FACTOR-α

目的 观察在地塞米松作用下, 肿瘤坏死因子 (TNF -α) 致痫大鼠海马GABAA受体表达的改变, 从而研究癫痫发病过程中内分泌和免疫调节相互关系的机制。方法 采用侧脑室分别注射 TNF- α、地塞米松 (Dex) +TNF- α以及生理盐水建立大鼠模型, 运用 SABC法进行免疫组化染色, 观察大鼠海马 GABAA受体表达的变化。结果 GABAA受体免疫反应主要定位于胞膜上。细胞计数及统计学处理表明: TNF- α组海马 CA1、CA3 区 GABAA受体阳性细胞数较对照组及Dex+TNF- α组显著减少 (P<0 . 01), 而对照组和Dex+TNF- α组无显著差异 (P>0. 05)。结论 地塞米松对 TNF- α致痫有抑制作用, 提示地塞米松的抑痫作用和TNF -α的致痫作用之一可能是通过调节抑制性氨基酸受体而实现的。

Objective To explore the interaction between the regulations of immune and endocrine systems in the mechanism of epilepsy, by observing the effects of dexamethasone on the expression of GABA A receptor immunoreactive cells in the hippocampus of rats with seizure induced by tumor necrosis factor α. Methods TNF-α protein, Dex + TNF-α protein, or saline was injected respectively into the lateral ventricle of the rats to establish the models. The method of SABC was used to detect the GABA A receptor positive cells in the hippocampus. Results Response to the immunization of GABA A receptors was mainly located on the cytomembrane. The results of cell counting and statistics indicated that less positive cells of GABA A receptor immunoreaction were found in the hippocampal area CA 1 and CA 3 of the TNF-α group (P<0. 01), while there was no obvious difference between the control and the Dex + TNF-α group (P>0. 05). Conclusion The results indicate that seizures induced by TNF-α can be inhibited by dexamethasone, and the adverse actions of TNF-α and dexamethasone on seizure may be realized by regulating the expression of GABA A receptors.