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目的 探讨糖皮质激素 (GC)的抗痫效应和抗痫机制。 方法 动物行为学观察和免疫细胞化学染色。 结果 戊四氮 (PTZ)可诱发癫痫大发作 ,如若在注入PTZ前 30min先注入地塞米松或苯妥英钠 (DPH)能减轻或抑制大鼠癫痫发作症状。免疫细胞化学染色结果表明 ,PTZ致痫组大鼠大脑皮质、海马回、齿状回有大量肥大的胶质原纤维酸性蛋白 (GFAP)阳性的星形胶质细胞。GC或DPH抗痫组GFAP免疫反应明显减弱 ,阳性细胞数量减少 ,突起短而少。Fos蛋白在PTZ组大鼠致痫后 1～ 1 5h有大量表达 ,而在上述两抗痫组显著少于PTZ致痫组。结论 1 通过与苯妥英钠 (传统抗痫药 )的抗痫效果相比较 ,进一步证明糖皮质激素具有抗痫效应。 2 糖皮质激素的抗痫机制可能与抑制星形胶质细胞的活动有关。 3 Fos蛋白表达的变化与癫痫活动有直接关系。
Objective To investigate the anti-epileptic effect and anti-epileptic mechanism of glucocorticoid (GC). Methods Animal behavior observation and immunocytochemical staining. Results Pentylenetetrazol (PTZ) induced epileptic seizures. Dexamethasone or phenytoin sodium (DPH) could reduce or inhibit seizure symptoms in rats 30 min before PTZ injection. Immunocytochemical staining results showed that a large number of hypertrophic glial fibrillary acidic protein (GFAP) -positive astrocytes were found in the cortex, hippocampus and dentate gyrus in rats with PTZ-induced epilepsy. The GFAP immunoreactivity in GC or DPH anti-epilepsy group was significantly weakened, the number of positive cells decreased, and the processes were shorter and fewer. Fos protein was abundantly expressed in PTZ group 1 ~ 15 hours after epileptic seizure, but was significantly less in PTZ group than in PTZ epilepsy group. Conclusions1 Further evidence of the anti-epileptic effect of glucocorticoids compared with the anti-epileptic effect of phenytoin sodium (traditional antiepileptic). 2 glucocorticoid antiepileptic mechanism may be related to inhibition of astrocyte activity. 3 Fos protein expression changes and epilepsy activity has a direct relationship.