当归芍药散活性部位JD-30对淀粉样β蛋白片段25-35抑制大鼠海马脑片CA1区长时程增强的改善作用

目的研究当归芍药散改善学习记忆能力的物质基础和作用机理。方法采用细胞外微电极记录技术,记录大鼠海马脑片CA1区群峰电位(PS)幅值和高频刺激诱发LTP后PS的增幅。结果用含当归芍药散活性部位JD-30(25,50和100mg.L-1)的人工脑脊液灌流大鼠海马脑片,其CA1区的PS幅值无明显变化。用相同浓度的JD-30孵育海马脑片90min以上并持续灌流,其CA1区高频刺激后的PS增幅与空白对照组相比无明显差异。而用Aβ25-35200nmo.lL-1处理的海马脑片CA1区高频刺激后的PS增幅受到明显抑制;若同时给予Aβ25-35和上述浓度的JD-30处理海马脑片,CA1区高频刺激后的PS增幅较Aβ25-35组升高,其中JD-30100mg.L-1组的PS增幅达到正常对照组水平。提示JD-30对正常海马脑片CA1区的基础突触传递和LTP没有影响,但可改善Aβ25-35所抑制的LTP。结论JD-30可改善神经突触可塑性,拮抗Aβ对LTP的抑制作用可能是其益智机制之一。

JD-30, an active constituent extracted from Danggui Shaoyao San,ameliorates amyloid beta-protein fragment 25-35 induced inhibition of long-term potentiation of CA1 area in rat hippocampal slices

AIM To study the material base and mechanism of cognition enhancing effect of Danggui Shaoyao San (DSS, also named Toki-shakuyaku-san in Japanese). METHODS By using extracellular microelectrode recording technique, population spike(PS) and long-germ potentiation(LTP) of CA1 area in hippocampal slices were induced and recorded. RESLUTSPerfused with JD-30(25, 50 and 100 mg·L^-1), an active constituent extracted from DSS, had no effect on PS amplitude of CA1 area in hippocampal slices. Incubated and perfused with the same concentrations of JD-30 had no effect on PS amplification of CA1 area after high frequency stimulation. Treatment with Aβ_25-35 200 nmol·L^-1 significant depressed PS amplification of CA1 area, and the inhibition by Aβ_25-35 was ameliorated by JD-30. Especially, JD-30 100 mg·L^-1 retrieved PS amplification to the normal group level. CONCLUSION JD-30 may improve synaptic plasticity, and it is possibly one of the mechanisms for its cognition enhancement action to amelioratethe inhibition of Aβ on LTP.