IL-1β对谷氨酸致痫大鼠大脑皮质、海马内蛋白激酶A表达的影响

EFFECTS OF IL-1β ON THE EXPRESSION OF PROTEIN KINASE A IN RATS WITH SEIZURE INDUCED BY L-GLUTAMATE

目的 探讨白细胞介素 1β (Interleukin 1beta ,IL 1β)对谷氨酸钠致痫大鼠脑内PKACβ表达的影响 ,为阐明IL 1β在致痫中的作用机制提供资料。方法 随机将健康成年SD大鼠分为对照组、Glu组、IL 1β +Glu组、IL 1ra +IL 1β +Glu组和MCCG (2 methyl 2 carboxycyclopropylglycine +IL 1β+Glu组 (每组 8只 )。采用行为学测试及WesternBlot和免疫组织化学方法观察。结果 MCCG组大鼠痫性发作潜伏期 [平均 (1 1± 0 2min) ]较Glu组 [平均 (2 0± 0 3min) ]及IL 1β +Glu组 [平均 (1 8± 0 2min) ]明显缩短 (P 0 0 5 ) ,痫性发作持续时间 [平均 (4 6 4± 1 6min) ]明显延长(P 0 0 5 ) ,且发作程度加重 ,对照组及IL 1ra +IL 1β +Glu组无痫性发作 ;WesternBlot结果显示PKACβ含量在Glu组和IL 1β +Glu组大鼠大脑皮质及海马内均较对照组和IL 1ra +IL 1β +Glu组明显增多 (P 0 0 5 ) ,而对照组和IL 1ra +IL 1β+Glu组两组间无明显差别 ,MCCG +IL 1β +Glu组PKACβ含量显著高于其余各组 (P 0 0 5 ) ;免疫组化染色显示 ,PKACβ免疫反应增强主要表现在大脑皮质、海马CA3区及齿状回的颗粒细胞层 ,其各组间的变化与WesternBlot结果一致。结论 IL 1β参与致痫 ,IL

? Objective To study the influence of IL-1β on the expression of protein kinase A β catalysis subunit (PKACβ) in rats with seizure induced by L-glutamate, and to investigatethe mechanism of IL-1β in the facilitation of seizure. Method Forty healthy mature male SD rats were randomly divided into 5 groups: Control group, Glu group, IL-1β+Glu group, IL-1ra+IL-1β+Glu group and MCCG+IL-1β+Glu group. Behaviour observation was carried out during the establishment of the models. Immunohistochemical staining and Western blot were used to assess the changes in the expression of PKACβ in the brain. Result The latent period and the time span of the seizure in the MCCG+IL-1β+Glu group with more serious seizure activities (Ⅳ-Ⅴgrade) (an average of 1.1±0.2 min and 46.4±1.6 min respectively) were remarkably reduced or prolonged when compared with those of the Glu group (an average of 2.0±0.3 min and 21.0±1.3 min respectively) and the IL-1β+Glu group (an average of 1.8±0.2 min and 22.5±1.5 min respectively). The control group and the IL-1ra+IL-1β+Glu group showed no seizure activities. Western Blot showed that the amount of PKACβ was increased in the Glu group and the IL-1β+Glu group in both the cortex and the hippocampus when compared with that of the control group and the IL-1ra+IL-1β+Glu group, with no significant difference between the latter two groups. Immunolabelling of PKACβ in the MCCG+IL-1β+Glu group was the highest in the above two brain regions. The increase of the immunohistochemical staining of PKACβ was mainly in the cortex, the hippocampal CA3 and the granular cell layer of the dentate gyrus, which coincided with the results of Western blotting. Conclusion IL-1β plays a role in the facilitation of seizure and PKA-induced signal transduction is involved in this process. 〔