1 Institute of Chinese Medicine, Heilongjiang University of Chinese Medicine, Harbin, China.
2 Department of Organic Chemistry, School of Pharmacy, Mudanjiang Medical University, Mudanjiang, China.
Rejuvenation Res. 2019 Apr;22(2):131-137. doi: 10.1089/rej.2018.2080. Epub 2018 Aug 29.
Kaixin-San (KXS), a Chinese formula, was used to treat "amnesia," a senile dementia in the modern world. This formula was reported to improve behavioral performances in many animal models. This study was designed to explore how KXS has improved amyloid-β (Aβ)-induced memory dysfunction in mice. The mouse models were achieved through unilateral ventricle injection with Aβ. The effects of KXS on memory improvement were evaluated by the step-down test. The electrophysiological changes induced by KXS were measured by long-term potentiation (LTP) analysis in the hippocampus . The expression of glutamate receptor 2 (GluR2) was observed through immunohistochemical staining. Behavioral experiment outcome demonstrated reduced avoidance time and increased error time during the step-down test in the mice of Aβ group. This memory impairment, however, was reversed by KXS. Electrophysiological experiment showed no significant difference between Aβ group and KXS group either in the size or the shape of field excitatory postsynaptic potentiation recorded from perforant path to dentate gyrus pathway. However, LTP in this region was reduced by Aβ and recovered by KXS administration. Moreover, immunohistochemical staining showed increased postsynaptic GluR2 expression in DG area in KXS group. These findings suggest that Aβ results in impairment to memory function of the animals, and KXS protects the animal from memory loss by rescuing LTP through postsynaptic mechanism which refers to increasing GluR2 expression.
开心散（KXS）是一种中药方剂，用于治疗现代世界的“健忘症”，即老年性痴呆。该方剂据报道能改善许多动物模型的行为表现。本研究旨在探讨 KXS 如何改善 Aβ诱导的小鼠记忆功能障碍。通过侧脑室注射 Aβ建立小鼠模型。通过跳台试验评估 KXS 对改善记忆的作用。通过在海马体中进行长时程增强（LTP）分析来测量 KXS 引起的电生理变化。通过免疫组织化学染色观察谷氨酸受体 2（GluR2）的表达。行为实验结果表明，Aβ组小鼠在跳台试验中逃避时间减少，错误时间增加。然而，KXS 逆转了这种记忆损伤。电生理实验显示，Aβ组和 KXS 组之间在从穿通通路到齿状回通路记录的场兴奋性突触后电位增强的大小或形状方面没有显著差异。然而，Aβ降低了该区域的 LTP，而 KXS 给药则恢复了 LTP。此外，免疫组织化学染色显示 KXS 组 DG 区突触后 GluR2 表达增加。这些发现表明，Aβ导致动物的记忆功能受损，而 KXS 通过增加突触后 GluR2 表达来挽救 LTP，从而保护动物免受记忆丧失。
