姜黄素对匹罗卡品致痫大鼠海马S100B蛋白表达的影响

目的:观察氯化锂-匹罗卡品致痫大鼠海马组织S100B表达,探讨姜黄素对癫痫大鼠神经保护作用机制。方法:动物随机分为3组,空白对照组、癫痫组、姜黄素治疗组。癫痫模型采用氯化锂-匹罗卡品诱导大鼠癫痫持续状态(SE),给药SE后予姜黄素300 mg/kg腹腔,大鼠癫痫造模后24 h和72 h取海马组织,苏木素-伊红(HE)染色观察海马组织病理形态学变化,免疫组化染色和免疫印迹法检测海马组织S100B蛋白的表达。结果:癫痫组海马神经元脱失和损伤明显,姜黄素治疗组明显减轻;与对照组相比,海马神经元S100B免疫反应阳性表达增加,差异显著(P<0.05);与模型组比较姜黄素治疗组海马神经元S100B阳性表达水平降低,差异显著(P<0.05)。结论:姜黄素治疗可降低匹罗卡品致痫大鼠海马神经元S100B蛋白表达,可能通过抑制星形胶质细胞活化来减轻癫痫发作脑损伤发挥神经保护作用。

Effect of Curcumin on Expression of S100B Protein in Hippocampus after Pilocarpine-Induced Status Epilepticus in Rats

Objective： To observe the expression of S100 B protein in the hippocampus after lithium- pilocarpine- induced status epilepticus in rats and investigate the neuroprotecive mechanism of curcumin against seizures impairment in rats. Methods： Rats were randomly divided into three groups; control group,epilepsy group,curcumin- treated group. Epileptic rats were generated using lithium – pilocarpine- induced status epilepticus（ SE）. Rats were given an intraperitoneal（ i. p.） injection of curcumin at a dose of 300 mg / kg after lithium pilocarpine treatment. Rats were sacrificed 24 h and 72 h after pilocarpin treatment. The hippocampus was removed and collected. The pathological changes observed in hippocampal tissue stained with hematoxylin- eosin（ HE）. Expression of S100 B protein in hippocampal tissue was detected by immunohistochemical staining and Western blotting. Result： Neuron loss and neuronal injury in epilepsy group was more severe than that in curcumin- treated group. The number of s100 B positive cell in the seizure group was significantly higher than that in the control group（ P〈0. 05）. The number of s100 B positive cell in curcumin- treated group was significantly lower than that in the seizure group（ P〈0. 05）. Conclusion： Inhibition of astrocyte activation is a possible neuroprotective mechanism of curcumin against seizures impairment in rats.