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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。
Objective: To explore the mechanism of estrogen (E) and curcumin (C) affecting epileptic seizures. Methods: The ovariectomized female rats were treated continuously with E and C for 5 days. The rats were killed on the 6th day by the kainic acid (KA) amygdala. The behavioral findings of epileptic seizures were observed The expression of c-Jun protein in hippocampus was detected by immunohistochemistry. Results: The severity of severe seizures in E plus C group (EC + KA group) was significantly lower than that in E + KA group (P <0.05). The expression of c-Jun protein in hippocampus of E + KA group was the highest, while that in C + KA group and control group (KA group) was less and no difference was found. Expression of c-Jun protein in hippocampus of EC + KA group Compared with E + KA group was significantly reduced (P <0.05). CONCLUSION: C can relieve the aggravation of epileptic seizures induced by E to a certain extent. It may inhibit E-AP-1 pathway by inhibiting the activity of c-Jun / activate-protein1 (AP-1) Blocked, thereby reducing the E-induced neuronal excitability.