The effects of Danggui-Shaoyao-San on neuronal degeneration and amyloidosis in mouse and its molecular mechanism for the treatment of Alzheimer’s disease

Cong Yang^1,2,†, You-Sheng Mo^1,2,†, Hui-Fang Chen^1,2, Yan-Hui Huang^1,2, Shao-Ling Li^1,2, Hong Wang¹, Shui-Qing Huang^1,2, Xiang Chang³, Qun Du^1,*, Qi Wang^1,2,*

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¹ Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, 510405 Guangzhou, Guangdong Province, China

² Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, 510405 Guangzhou, Guangdong Province, China

³ Xi’an Hospital of Traditional Chinese Medicine, 710021 Xi’an, Shaanxi Province, China

^*Correspondence: duqun@gzucm.edu.cn (Qun Du); wangqi@gzucm.edu.cn (Qi Wang)
^† These authors contributed equally.

J. Integr. Neurosci. 2021, 20(2), 255–264; https://doi.org/10.31083/j.jin2002025

Submitted: 30 September 2020 | Revised: 6 December 2020 | Accepted: 1 February 2021 | Published: 30 June 2021

This is an open access article under the CC BY 4.0 license (https://creativecommons.org/licenses/by/4.0/).

Abstract

The abnormal deposition of the extracellular amyloid- $\beta$ peptide is the typical pathological hallmark of Alzheimer’s disease. Strategies to reduce the amyloid- $\beta$ deposition effectively alleviate the neuronal degeneration and cognitive deficits of Alzheimer’s disease. Danggui-Shaoyao-San has been considered a useful therapeutic agent known for the treatment of Alzheimer’s disease. However, the mechanism of Danggui-Shaoyao-San for the treatment of Alzheimer’s disease remains unclear. We investigated Danggui-Shaoyao-San’s effect on amyloidosis and neuronal degeneration in an APP/PS1 mouse model. We found Danggui-Shaoyao-San alleviated the cognitive deficits in APP/PS1 mice. Additionally, Danggui-Shaoyao-San ameliorated the neuronal degeneration in these mice. Danggui-Shaoyao-San reduced the amyloidosis and amyloid- $\beta_{1-42}$ deposition in APP/PS1 mouse brain and down-regulated the receptor for advanced glycation end products, and up-regulated the level of low-density lipoprotein receptor-related protein-1. However, the protein expression of the $\beta$ -amyloid precursor protein, $\beta$ -Secretase and presenilin-1 (PS1) in the amyloid- $\beta$ production pathway, and the expression of neprilysin and insulin-degrading enzyme in the amyloid- $\beta$ degradation pathway were not altered. Our findings collectively suggest that Danggui-Shaoyao-San could ameliorate the amyloidosis and neuronal degeneration of Alzheimer’s disease, which may be associated with its up-regulation lipoprotein receptor-related protein-1 and down-regulation of the receptor for advanced glycation end products.

Keywords

Danggui-Shaoyao-San

Alzheimer's disease

Cognitive deficits

Amyloidosis

Lipoprotein receptor-related protein-1

RAGE

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Fig. 1.

DSS alleviates the cognitive disorders in APP/PS1 mice. (A–D) Morris water maze test: Escape latency (A) and pathway (B) during platform trials, time spent in the target quadrant (C) and the number of crossing through the platform (D) in the probe test. Percentage of alternation (E) in the Y-maze test. The time spent in the central area (F) in the open field test. The escape latency was shown as mean $\pm$ SEM. Other data were shown as mean $\pm$ SD. Compared with the control group, ${}^{\#}$ P $<$ 0.05 or ${}^{\#\#}$ P $<$ 0.01, compared with the model group, *P $<$ 0.05 or **P $<$ 0.01. N = 10~12 in each group.

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J. Integr. Neurosci. Print ISSN 0219-6352 Electronic ISSN 1757-448X