764-3对脑损伤所致认知障碍的改善作用及作用机理

Beneficial Effect and Mechanism of 764-3 on Cognitive Deficit Induced by Brain Damage in Rats

用海人酸损伤大鼠双侧尾核并经多种行为学测定，成功地建立了兴奋毒性损伤所致认知障碍模型；观察到中药单体764－3（8mg／（kg·d），ip）能够明显改善尾核损伤大鼠的学习记忆缺陷，并减轻兴奋毒性所致的尾核神经元缺失。拮抗兴奋毒性所致神经细胞膜Na+－K+－ATP酶和Ca2+－Mg2+－ATP酶活性下降。可能是764－3的部分作用机理。

Animal model of excitotoxic cognitive deficit induced by kainic acid bilaterally injectioninto caudate nucleus was successfully established in rats. Based on this model, chronic ad-ministration of 764-3 (8 mg/(kg. d), ip), an extract from Chinese traditiona1 medicine,markedly improved the learning and memory impairment in the injured caudate nucleus rats-Moreover, attenuation of the neuronal loss in caudate nucleus following excitotoxic damagewas observed after 764-3 treatment. In addition, results indicated that the mechanism of theeffect of 764-3 may be related to the antagonism against the decline of Na+-K+-ATPase andCa2+-Mg2+-ATPase actlvlty in synaptlc membrane resulted from excitotoxicity.