还少丹的脑保护机制研究

目的：为探讨中药古成方“还少丹”的脑保护机制，观察了该药对脑兴奋性损伤模型的预防及治疗作用。方法：利用小鼠双侧颈总动脉结扎及反复再灌的手术造成小鼠智力下降（避暗实验次数增多）的脑损伤模型，从行为学方面观察了还少丹对脑损伤小鼠学习记忆能力的改善作用，并进一步利用受体研究方法考察了该药的脑保护机制。结果：还少丹可明显减少术后小鼠避暗实验的错误次数（模型组为２．００±０．３４次／５ｍｉｎ，单纯治疗组为０．７５±０．２５次／５ｍｉｎ，Ｐ＜０．０１；预防加治疗组为０．３８±０．１８次／５ｍｉｎ，Ｐ＜０．０１）。受体结合实验表明，还少丹明显抑制小鼠脑损伤后引起的大脑皮层、海马两部位Ｎ－甲基－Ｄ－天冬氨酸（即ＮＭＤＡ）受体的激活，与模型组比较，有明显差异（Ｐ均＜０．０１）；同时发现用药后胆碱乙酸化转移酶（ＣＡＴ）的活性明显提高（Ｐ＜０．０１）。结论：揭示该药具有对抗兴奋性氨基酸毒性的作用。还少丹还可明显增强脑损伤模型的皮层、海马部位的ＣＡＴ活性。

英文摘要:

Objective:To observe the protective effect of Huanshaodan(HSD) in mouse brain in a steady ischemia-reperfusion model. Methods: Step-through experiment, receptor binding test and choline acetyl-transferase (CAT) activity detemination was performed. Results: After HSD treatment, mice made much less mistakes in step-through experiment than sham grouPS. Meanwhile the 3H-MK801 binding of cerebral cortex and hippocampus tissues was significantly decreased. CAT activity Of cerebral cortex and hippocampus tissue were increased respectively. COnclusion: HSD might antagonize ischemia injury of brain through modulating excessive activation of glutamate N-methyl-D-Aspartic acid receptors.

关闭