摘要
研究BmKE的抗癫痫作用及其机制。观察戊四氮(PTZ)致癫痫模型小鼠,丙戊酸钠(VAP)对照治疗组和BmKE高(BmKEH)、中(BmKEM)、低(BmKEL)剂量治疗组小鼠癫痫发作的潜伏期;应用同位素3H标记MK-801检测小鼠大脑皮层兴奋性N-甲基-D-门冬氨酸受体(NMDAR)结合活性。结果发现,VAP和BmKEM能显著延长PTZ致癫痫小鼠的发作潜伏期(p<0.05)。PTZ致癫痫小鼠大脑皮层的NMDAR结合活性比正常对照组升高了18%(p<0.05),经治疗的VAP和BmKEL组小鼠大脑皮层NMDAR结合活性明显降低(p<0.05),分别降低了14%和13%,BmKEM和BmKEH均显著降低癫痫小鼠大脑皮层NMDAR结合活性(p<0.001),分别降低了49%和53%。BmKE对大脑皮层的兴奋性NMDAR的抑制作用呈剂量相关性。
Reviews the antiepileptic effect of Buthus martensic Karch Extract（BmKE） and its mechanism, involving the observation of latent periods of FIE-induced epileptic mice, of latent periods of vaproate sodium（VAP, positive control drug）-induced ones （ ineoraparison group ） and latent periods of ones in BmKE （ H ）, BmKE （ M ）, BmKE （L） comparison groups, as well as the application of isotope ^3H-tagged MK-801 to detect the excitative NMDA receptor （NMDAR） binding activity of cerebral cortex. As it turns out, VAP and BmKE （M） significantly prolong latent periods of epileptic mice（p 〈 0.05）. The prolonged value of latent periods of epileptic mice treated by BmKE（H） is 49% shorter than that treated by BmKE（M）. NMDAR binding activity in cerebral cortex of PTZ-indueed epileptic mice is 58% higher than that of nomal mice（p 〈 0.05）. NMDAR binding activities in cerebral cortex of epileptic mice treated by VAPand BmKE（L）, BmKE（M） and BmKE（H） are 14% and 13%（p 〈0.05）, and 49% and 53%（p 〈 0.001） lower than that of PTZ-indueed epileptic mice respectively. The inhibiting effect of BmKE NMDAR binding activities in cerebral cortex is relative to dosage.
出处
《北京联合大学学报》
CAS
2006年第4期50-52,共3页
Journal of Beijing Union University
