姜黄素抑制大鼠杏仁核点燃性癫痫发作。

Curcumin inhibits amygdaloid kindled seizures in rats.

作者信息

DU Peng, Li Xin, Lin Hao-Jie, Peng Wei-Feng, Liu Jian-Ying, Ma Yu, Fan Wei, Wang Xin

机构信息

Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.

出版信息

Chin Med J (Engl). 2009 Jun 20;122(12):1435-8.

PMID:19567167

Abstract

BACKGROUND

Curcumin can reduce the severity of seizures induced by kainate acid (KA), but the role of curcumin in amygdaloid kindled models is still unknown. This study aimed to explore the effect of curcumin on the development of kindling in amygdaloid kindled rats.

METHODS

With an amygdaloid kindled Sprague-Dawley (SD) rat model and an electrophysiological method, different doses of curcumin (10 mgxkg(-1)xd(-1) and 30 mgxkg(-1)xd(-1) as low dose groups, 100 mgxkg(-1)xd(-1) and 300 mgxkg(-1)xd(-1) as high dose groups) were administrated intraperitoneally during the whole kindling days, by comparison with the course of kindling, afterdischarge (AD) thresholds and the number of ADs to reach the stages of class I to V seizures in the rats between control and experimental groups. One-way or two-way ANOVA and Fisher's least significant difference post hoc test were used for statistical analyses.

RESULTS

Curcumin (both 100 mgxkg(-1)xd(-1) and 300 mgxkg(-1)xd(-1)) significantly inhibited the behavioral seizure development in the (19.80 +/- 2.25) and (21.70 +/- 2.21) stimulations respectively required to reach the kindled state. Rats treated with 100 mgxkg(-1)xd(-1) curcumin 30 minutes before kindling stimulation showed an obvious increase in the stimulation current intensity required to evoke AD from (703.3 +/- 85.9) microA to (960.0 +/- 116.5) microA during the progression to class V seizures. Rats treated with 300 mgxkg(-1)xd(-1) curcumin showed a significant increase in the stimulation current intensity required to evoke AD from (735.0 +/- 65.2) microA to (867.0 +/- 93.4) microA during the progression to class V seizures. Rats treated with 300 mgxkg(-1)xd(-1) curcumin required much more evoked ADs to reach the stage of class both IV (as (199.83 +/- 12.47) seconds) and V seizures (as (210.66 +/- 10.68) seconds). Rats treated with 100 mgxkg(-1)xd(-1) curcumin required much more evoked ADs to reach the stage of class V seizures (as (219.56 +/- 18.24) seconds).

CONCLUSION

Our study suggests that curcumin has a potential antiepileptogenic effect on kindling-induced epileptogenesis.

摘要

背景

姜黄素可减轻海藻酸（KA）诱导的癫痫发作严重程度，但姜黄素在杏仁核点燃模型中的作用仍不清楚。本研究旨在探讨姜黄素对杏仁核点燃大鼠点燃发展的影响。

方法

采用杏仁核点燃的Sprague-Dawley（SD）大鼠模型和电生理方法，在整个点燃期间腹腔注射不同剂量的姜黄素（低剂量组为10mg·kg⁻¹·d⁻¹和30mg·kg⁻¹·d⁻¹，高剂量组为100mg·kg⁻¹·d⁻¹和300mg·kg⁻¹·d⁻¹），通过比较对照组和实验组大鼠的点燃过程、后放电（AD）阈值以及达到Ⅰ至Ⅴ级癫痫发作阶段所需的AD次数。采用单向或双向方差分析以及Fisher最小显著差事后检验进行统计分析。

结果

姜黄素（100mg·kg⁻¹·d⁻¹和300mg·kg⁻¹·d⁻¹）分别在（19.80±2.25）次和（21.70±2.21）次刺激时显著抑制行为性癫痫发作的发展，从而达到点燃状态。在点燃刺激前30分钟用100mg·kg⁻¹·d⁻¹姜黄素处理的大鼠，在进展到Ⅴ级癫痫发作期间，诱发AD所需的刺激电流强度从（703.3±85.9）μA明显增加到（960.0±116.5）μA。用300mg·kg⁻¹·d⁻¹姜黄素处理的大鼠在进展到Ⅴ级癫痫发作期间，诱发AD所需的刺激电流强度从（735.0±65.2）μA显著增加到（867.0±93.4）μA。用300mg·kg⁻¹·d⁻¹姜黄素处理的大鼠达到Ⅳ级（为（199.83±12.47）秒）和Ⅴ级癫痫发作阶段（为（210.66±10.68）秒）所需的诱发AD次数更多。用100mg·kg⁻¹·d⁻¹姜黄素处理的大鼠达到Ⅴ级癫痫发作阶段（为（219.56±18.24）秒）所需的诱发AD次数更多。