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目的 探讨脑内一氧化氮 (NO)介质对癫痫发作及白细胞介素 6(IL 6)表达的影响。方法 采用红藻氨酸 (KA)诱导大鼠癫痫发作 ,以一氧化氮合酶 (NOS)抑制剂L 硝基精氨酸 (L NNA)和NO前体L 精氨酸 (L Arg)进行干预 ,从行为学评估及形态学的角度 ,对KA癫痫发作和IL 6的相关变化做了观察。结果 一次惊厥剂量的KA (1 0mg·kg- 1 )可使动物发生明显的时间相关性癫痫发作 ,并伴随着海马结构、梨状区及大脑皮层等相关脑区IL 6免疫反应(IL 6ir)的快速升高与增强。而经L NNA(50mg·kg- 1 )或与其等摩尔量的L Arg(40mg·kg- 1 )预处理后 ,其癫痫行为发生了明显变化。L NNA促进和加重了癫痫发作 ,KA给药后 3h许多动物死亡 ,而L Arg可使癫痫发作行为减缓。与行为干预相对应 ,L NNA对海马结构等相关脑区内的IL 6ir有明显的上调作用 ,L Arg则显示出相反的效应。结论 内源性NO介质对KA癫痫发作具有抑制作用 ,对IL 6的快速表达具有下调作用 ,但这种下调作用与内源性NO介质抗癫痫发作的稳态关系还需进一步探讨
Objective To investigate the effects of nitric oxide (NO) in brain on the seizure and the expression of interleukin 6 (IL 6) in brain. Methods Kainate (KA) -induced epileptic seizures were induced in rats by nitric oxide synthase (NOS) inhibitor L-nitro-arginine (L-NNA) and NO-L arginine , From the behavioral assessment and morphological point of view, KA seizures and IL 6 related changes were observed. Results A convulsant dose of KA (10 mg · kg -1) produced significant time-related seizures in animals accompanied by IL 6 immunoreactivity (IL 6ir) in the hippocampus, corpus striatum and cerebral cortex, Rapid rise and increase. However, pretreatment with L-NNA (50 mg · kg-1) or its equimolar amount of L Arg (40 mg · kg-1) significantly changed the epileptic behavior. L NNA promotes and aggravates seizures, and many animals die 3 hours after KA administration, while L Arg slows seizure behavior. Corresponding to behavioral intervention, L-NNA significantly upregulated IL-6ir in the hippocampal formation-related brain regions, while L-Arg showed the opposite effect. Conclusions Endogenous NO mediator has inhibitory effect on KA seizures and down-regulates the rapid expression of IL-6. However, this down-regulation and the steady-state relationship between endogenous nitric oxide and antiepileptic need to be further explored