摘要
目的:探讨依达拉奉抗癫痫的机制。方法:应用SP法研究戊四氮致癫痫大鼠和褪黑素抗癫痫大鼠海马谷氨酸受体ζ1(Nmethyl—D—aspartate recepterζ1,NMDAζ1)和,γ-氨基丁酸受体Aαl(γ-aminobutyricacid—Arecepterαl,GABAARcd)的变化。结果:海马NMDAζ1的表达在戊四氮致癫痫组明显高于正常对照组(P〈0.01),依达拉奉抗癫痫组明显低于戊四氮致癫痫组(P〈0.01),依达拉奉抗癫痫组与正常对照组之间差异无显著性意义(P〉0.05);海马GABAARcd的表达在戊四氮致癫痫组明显低于正常对照组(P〈0.01),依达拉奉抗癫痫组明显高于戊四氮致癫痫组(P〈0.01),依达拉奉抗癫痫组与正常对照组之间差异无显著性意义(P〉0.05)。结论:依达拉奉可能通过抑制海马兴奋性神经递质受体NMDAαl和激活海马抑制性神经递质受体GABAARcd的活性与表达,降低大脑皮质的兴奋性,抑制癫痫的形成及发展来发挥抗癫痫作用。
Objective: To explore the possible antiiepileptic mechanism of edaravone. Methods: The expressions of N - methyl - D - aspartate receptorζ1( NMDAζ1 ) and γ- aminobulyric acid - A receptororα(GABAARαl) in the hippocampus of pentylenetetrazole (PTZ) -induced epileptic rats and epileptic rats treaded with edaravone were determined by SP method. Results: The expression of NMDAζ1 in the hippocampus of PTZ group rats was higher than that of control group rats. After treatment with edaravone, the NMDAζ1 expression was decreased significantly. There was no significant difference in the expression of NMDAζ1 between the rats of edaravone group and normal control group. The expression of GABAARαl in the hippocampus of PTZ group rats was lower than that of control group rats. After treatment with edaravone, the expression of GABAARαl was increased significantly. There was also no significant difference between the rats of edaravone group and normal control group. Conclusions: edaravonc may reduce the excitability of cere- bral cortices by inhibiting the activities of NMDAζ1 and by promoting the activities of GABAARod in the hippocampus, so the development and formation of epilepsy are inhibited.
出处
《中国民康医学》
2009年第5期435-436,440,共3页
Medical Journal of Chinese People’s Health
关键词
癫痫
依达拉奉
N-甲基-D-天冬氨酸受体
Γ-氨基丁酸受体
戊四氮
epilepsy
Edaravone
N - methyl - D - aspartate receptertate
γ - aminobutyric acid - A rece acid-A recepteral
Pentylenetetrazole