文献类型：期刊文献

中文题名：东亚钳蝎提取物对癫痫小鼠大脑皮层NMDA受体和GABA_A受体的调节作用

英文题名：The Modulation of Buthus martensic Karch Extract (BmKE) on Cerebral Cortex NMDA Receptor and GABA_A Receptor in Epileptic Mice

作者：黄迎春[1];左萍萍[2]

第一作者：黄迎春

机构：[1]北京联合大学生物化工学院;[2]中国医学科学院中国协和医科大学

第一机构：北京联合大学生物化学工程学院

年份：2007

卷号：18

期号：1

起止页码：71-73

中文期刊名：时珍国医国药

外文期刊名：Lishizhen Medicine and Materia Medica Research

收录：北大核心:【北大核心2004】；CSCD:【CSCD_E2011_2012】；

语种：中文

中文关键词：东亚钳蝎提取物;GABA受体;NMDA受体;癫痫

外文关键词：BroKE; GABAA receptor; NMDA receptor; Convulsion latent period

摘要：目的研究BmKE对抗戊四氮致癫痫作用及其对致痫小鼠大脑皮层NMDAR和GABAAR的调节作用。方法观察戊四氮(PTZ)致癫痫模型小鼠,丙戊酸钠(VAP,阳性对照)治疗组和BmKE低(L)、中(M)、高(H)剂量治疗组小鼠癫痫发作的潜伏期,应用同位素3H分别标记MK-801和Muc imol,检测小鼠大脑皮层NMDAR和GABAAR的结合活性。结果BmKE(M)能显著延长PTZ致癫痫小鼠的发作潜伏期(P<0.05),BmKE(L)作用很小,BmKE(H)治疗组癫痫小鼠发作潜伏期的延长值比BmKE(M)治疗组低。PTZ显著升高致痫小鼠大脑皮层的NMDAR结合活性(P<0.05),BmKE(L)治疗组小鼠大脑皮层NMDAR结合活性降低,但是无显著性差异,BmKE(M)和BmKE(H)均极显著降低癫痫小鼠大脑皮层NMDAR结合活性(P<0.001)。BmKE(L)和BmKE(H)显著提高GABAAR结合活性(P<0.05),BmKE(M)极显著提高GABAAR结合活性(P<0.001)。结论适量的BmKE能够有效治疗戊四氮引起的癫痫,显著延长癫痫小鼠的发作潜伏期,BmKE抗癫痫的作用机理,可能与其抑制NMDAR结合活性,激活GABAAR的结合活性有关。
Objective To study the antagonism of BmKE on epilepsy of PTZ-induced epileptic mice and the modulation on NMDA receptor（NMDAR） and GABAA receptor （GABAAR） binding activities in cerebral cortex. Methods The convulsion latent periods of FIE-induced epileptic mice, vaproate sodium （ VAP, positive control drug） treating group and BmKE （ L ）, BmKE （ M ）, BmKE （H） treating groups were observed. NMDAR and GABAAR binding activities of cerebral cortex were detected by isotope 3H - tagged MK - 801 and mulimol respectively. Results BmKE （M） significantly prolonged laten periods of epileptic mice （ P 〈 0.05 ）, BmKE（L） had a few effect on latent periods, the prolonged value of latent periods treated by BmKE（H） was shorter than that treated by BmKE（M）. PTZ significantly increased NMDAR binding activities in cerebral cortex of mice （P 〈 0.05 ）. Both BmKE（M） and BmKE（H） excessively decreased those of PTZ - induced epileptic mice（ p 〈 0. 001 ）, but those of BmKE（L） treated group had no significant difference with those of FIE-induced epilepsic mice. GABAAR binding activities were reduced by PTZ. （P 〈 0. 005）. BmKE （L） and BmKE （ H ） significantly increased those of PTZ-induced epileptic mice （ P 〈 0.05 ）, and BmKE（M） excessively increased those of PTZ-induced epileptic miee（P 〈0.001 ）. Conclusion Suitable BmKE can prolong latent periods of epilepstic mice induced by PTZ, and has an antiepileptic effect. The effects of BmKE may have relationship between the inhibition on NMDAR binding avtivities and excitation on GABAAR binding avtivities in cerebral cortex of epileptic mice.