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. 2021 Dec;59(1):311-320.
doi: 10.1080/13880209.2021.1900879.

Aconiti lateralis Radix Praeparata inhibits Alzheimer's disease by regulating the complex regulation network with the core of GRIN1 and MAPK1

Yutao Wang  1   2 , Huixiang Zhang  3 , Jing Wang  4 , Ming Yu  5 , Qianqian Zhang  2 , Shan Yan  5 , Dingyun You  6 , Lanlan Shi  2 , Lihuan Zhang  1 , Limei Wang  1 , Hongxiang Wu  7 , Xue Cao  1
Affiliations

Aconiti lateralis Radix Praeparata inhibits Alzheimer's disease by regulating the complex regulation network with the core of GRIN1 and MAPK1

Yutao Wang et al. Pharm Biol. 2021 Dec.

Abstract

Context: Current medicine for Alzheimer's disease (AD) cannot effectively reverse or block nerve injury. Traditional Chinese Medicine practice and research imply Aconiti lateralis Radix Praeparata (Fuzi) may meet this goal.

Objective: Analysing the anti-AD effect of Fuzi and its potential molecular mechanism.

Materials and methods: AD model cells were treated with Fuzi in 0-300 mg/mL for 24 h in 37 °C. The cell viability (CV) and length of cell projections (LCP) for each group were observed, analysed, and standardised using control as a baseline (CVs and LCPs). The Fuzi and AD relevant genes were identified basing on databases, and the molecular mechanism of Fuzi anti-AD was predicted by network analysis.

Results: Experiment results showed that Fuzi in 0.4 mg/mL boosted LCP (LCPs = 1.2533, p ≤ 0.05), and in 1.6-100 mg/mL increased CV (CVs from 1.1673 to 1.3321, p ≤ 0.05). Bioinformatics analysis found 17 Fuzi target genes (relevant scores ≥ 20), showing strong AD relevant signals (RMS_p ≤ 0.05, related scores ≥ 5), enriched in the pathways regulating axon growth, synaptic plasticity, cell survival, proliferation, apoptosis, and death (p ≤ 0.05). Especially, GRIN1 and MAPK1 interacted with APP protein and located in the key point of the "Alzheimer's disease" pathway.

Discussion and conclusions: These results suggest that Fuzi may have therapeutic and prevention potential in AD, and GRIN1 and MAPK1 may be the core of the pathways of the Fuzi anti-AD process. Fuzi should be studied more extensively, especially for the prevention of AD.

Keywords: APP cells; Fuzi; aminophenol; therapy.

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Conflict of interest statement

The authors report no declarations of interest. The authors alone are responsible for the content and writing of the paper.

Figures

Figure 1.
Figure 1.
The gene interaction and the change pattern of cells. (A) The modification pattern for the cell viability and the length of cell’s projections, when APP cells were treated by Fuzi solution of different concentration. Statistically (p ≤ 0.05) and extremely (p ≤ 0.01) significant difference were symbolled as “*” and “**”, and p ≤ 0.1 was symbolled as “#”. (B) The gene interaction pattern for the AD relevant Fuzi target genes.
Figure 2.
Figure 2.
The microscope images for cell morphology. NC symbol the APP cells were not treated by Fuzi. The other images symbol the APP cells were treated by Fuzi solution of different concentration, from 0.4 to 300 mg/ml.
Figure 3.
Figure 3.
The KEGG pathway of AD.
Figure 4.
Figure 4.
The relationship of 17 candidate genes and 4 compounds (m-aminophenol, o-aminophenol, p-aminophenol, and coryneine) related genes. (A) The crossover relationship of the genes. (B) The crossover relationship of enrichment pathways that the genes enriched in.
See this image and copyright information in PMC

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