姜黄素对氯化锂-匹罗卡品诱导癫癎持续状态的预防作用

Preventive effects of curcumin on status epilepticus induced by lithium chloride-pilocarpine

目的探讨姜黄素对氯化锂-匹罗卡品诱导大鼠癫持续状态(SE)的预防作用及其神经元保护作用。方法Spra-gue-Daw ley(SD)大鼠45只随机均分成3组:预防组(n=15)、非预防组(n=15)和对照组(n=15)。观察各组SE的发生情况;SE后24 h,用焦油紫尼氏染色检查海马CA3区的存活神经元,用DNA片段原位末端标记技术(TUNEL)检查CA3区细胞程序化死亡情况。结果预防组SE发生率为66.7%,明显低于非预防组(100%)(P<0.05);预防组SE潜伏期为(41.0±18.1)m in,明显长于非预防组的(21.5±8.2)m in(P<0.01)。SE后24 h,CA3区存活神经元数量和程序化死亡细胞数量在预防组和非预防组间差异无统计学意义(P>0.05)。结论预先给予姜黄素能抑制氯化锂-匹罗卡品诱导的SE,但无明显神经元保护作用,其机制和潜在的临床应用价值值得深入研究。

Objective To investigate the preventive effects of curcumin for status epilepticus （SE） induced by lithium chloride-pilocarpine. Methods Totally 45 Sprague-Dawley （SD） rats were randomly divided into three groups： preventive group （ n = 15 ）, non-preventive group （ n = 15 ）, and control group （ n = 15 ）. The latency peroid and incidence of SE were recorded. The surviving neurons were stained by using nissl staining, and the programme death cells were detected by using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） in hippocampal CA3. Results The SE incidence of preventive group was 66. 7%, which was significantly lower than that of non-preventive group （ P 〈 0. 05 ）. The latency period of preventive group [ （41.0 ± 18. 1 ） min ] was longer than that of nonpreventive group [ （21.5 ±8. 2） min]. The numbers of surviving neurons and programme death cells showed no significant difference between the preventive group and non-preventive group （ P 〉 0. 05）. Conclusion Pretreatment of cureumin can prevent the SE induced by lithium chloride-pilocarpine and the pretreatment can not protect the neuron.