摘要
目的:探讨雌激素(E)和姜黄素(C)影响癫发作的机制。方法:用E和C单独及联用连续处理去势雌性大鼠5d,第6天以海人酸(KA)杏仁核点燃法制备癫大鼠模型,观察大鼠癫发作的行为学表现,用免疫组化方法检测海马组织c-Jun蛋白的表达。结果:E加C组(EC+KA组)大鼠癫重度发作的严重程度较E组(E+KA组)明显减轻(P<0.05)。E+KA组海马中c-Jun蛋白表达最多,C组(C+KA组)及对照组(KA组)均表达较少且没有任何差异;EC+KA组海马的CA1区c-Jun蛋白表达较E+KA组明显减少(P<0.05)。结论:C能一定程度上减轻E引起的癫发作加重,它可能通过抑制c-Jun/核转录因子激活蛋白-1(activate-protein1,AP-1)活性,使E作用的AP-1通路受阻,从而减轻了E的促神经元兴奋作用。
Aim： To explore the mechanism of epileptic seizure affected by estrogen and curcumin. Methods： The ovariotomized rats were treated for five days with estrogen and/or curcumin, and at the sixth day the rats were induced to become epilepsy by kainic acid （KA） introamgydale injection. The behaviors of epileptic seizured rats were observed, and their c-Jun protein expressions in the hippocampus were measured by using immuno-histochemical method. Results： Comparing the serious degree of heavy epileptic seizure, the rats treated with estrogen and curcumin together （EC＋KA group） were less than the rats treated with estrogen alone （E ＋KA group）. The most expression of c-Jun protein in hippocampus was observed in the E＋KA group and lesser the protein expression was in the C＋KA group （rats treated with curcumin） and KA group （control group）, and the protein expression was not any significant difference. In addition, the expression of c-Jun protein in the hippocampal CA1 subfield in the EC＋KA group was much less than that in the E＋KA group. Conclusion： Curcumin could alleviate the seizures exacerbated by estrogen （P 〈 0.05）. A possible mechanism was that curcumin inhibited the gateway of activate-proteinl （AP-1） through making c-Jun/AP-1 inactivation, which decreased the neuron excitability induced by estrogen.
出处
《中国临床神经科学》
2007年第6期578-582,共5页
Chinese Journal of Clinical Neurosciences
基金
复旦大学青年科学基金资助(2005年)
