摘要
目的探讨姜黄素对大鼠癫痫持续状态(SE)后海马神经元程序化死亡的影响。方法SD大鼠90只随机均分入癫痫组、姜黄素治疗组和对照组。建立氯化锂-匹罗卡品大鼠SE模型。应用DNA片段原位末端标记技术(TUNEL)观察SE后2h、4h、6h、24h、72h海马CA1区和CA3区TUNEL阳性细胞数的动态变化。结果对照组未见TUNEL阳性细胞。TUNEL阳性细胞主要分布在CA1区和CA3区。SE组TUNEL阳性细胞数在SE后6h开始增加(P<0.01),24h达高峰,72h较24h下降,姜黄素治疗组与SE组TUNEL阳性细胞数的动态变化趋势类似,但姜黄素治疗组SE后6h、24h、72h的阳性细胞数显著减少(P<0.01)。结论姜黄素能防治SE后海马神经元程序化死亡。
Objective：To investigate the influence of curcumin ter status epilepticus（SE）.Method：90 Sprague-Dawley（SD） rats on the programme cell death in rat hippocampus afwere randomly enrolled into the control group（n=30）, SE group （n=30） or curcumin treated group. The lithium-piloearpine induced SE was used as the SE model. The programme death cells in CA1 and CA3 were detected dynamically by TUNEL.Result：No TUNEL positive cell was observed in the control group. The number of TUNEL positive cells, presenting mainly in CA1 and CA3, increased 6 hours after SE（P〈0.01）and reached a peak 24 hours after SE, then got a little degression（P〈0.01） for both SE group and curcumin treated group. However, the numbers of TUNEL positive cells in curcumin treated group were notably fewer than those in SE group at the time point of 6h,24h ,72h after SE, respectively （P〈0.01）.Conclusion： The curcumin can prevent hippocampal neurons from programme cell death after SE.
出处
《中国康复医学杂志》
CAS
CSCD
北大核心
2006年第7期590-592,共3页
Chinese Journal of Rehabilitation Medicine
基金
教育部高等学校优秀青年教师教学科研奖励计划(2001-182)
教育部博士点基金(20030533042)
