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Discovery of an evodiamine derivative for PI3K/AKT/GSK3β pathway activation and AD pathology improvement in mouse models.

作者信息

Pang Shuo, Li Siyuan, Cheng Hanzeng, Luo Zhuohui, Qi Xiaolong, Guan Feifei, Dong Wei, Gao Shan, Liu Ning, Gao Xiang, Pan Shuo, Zhang Xu, Zhang Li, Yang Yajun, Zhang Lianfeng

机构信息

Key Laboratory of Human Disease Comparative Medicine, National Health Commission of China (NHC), Institute of Laboratory Animal Science, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.

Beijing Engineering Research Center for Experimental Animal Models of Human Diseases, Institute of Laboratory Animal Science, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.

出版信息

Front Mol Neurosci. 2023 Jan 9;15:1025066. doi: 10.3389/fnmol.2022.1025066. eCollection 2022.

DOI:10.3389/fnmol.2022.1025066
PMID:36698780
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9868638/
Abstract

Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive neurodegeneration and cognitive decline. Evodiamine, a main component in Chinese medicine, was found to improve cognitive impairment in AD model mice based on several intensive studies. However, evodiamine has high cytotoxicity and poor bioactivity. In this study, several evodiamine derivatives were synthesized heterocyclic substitution and amide introduction and screened for cytotoxicity and antioxidant capacity. Under the same concentrations, compound was found to exhibit lower cytotoxicity and higher activity against HO and amyloid β oligomers (AβOs) than evodiamine and significantly improve the working memory and spatial memory of 3 x Tg and APP/PS1 AD mice. Subsequent RNA sequencing and pathway enrichment analysis showed that affected AD-related genes and the AMPK and insulin signaling pathways. Furthermore, we confirmed that recovered PI3K/AKT/GSK3β/Tau dysfunction and . In conclusion, represents a potential lead compound for AD therapy based on the recovery of PI3K/AKT/GSK3β pathway dysfunction.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/02247c8410f5/fnmol-15-1025066-g0010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/f71d5747c4e2/fnmol-15-1025066-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/ecf0d8c3b43a/fnmol-15-1025066-g0011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/2e42de2a5611/fnmol-15-1025066-g0012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/3f2e017ba3a9/fnmol-15-1025066-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/7e37164a363b/fnmol-15-1025066-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/d5aa184ec988/fnmol-15-1025066-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/8c93a93df9bd/fnmol-15-1025066-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/722374caf230/fnmol-15-1025066-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/e96b95058ae2/fnmol-15-1025066-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/ce277adb715e/fnmol-15-1025066-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/fcafdce34d72/fnmol-15-1025066-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/02247c8410f5/fnmol-15-1025066-g0010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/f71d5747c4e2/fnmol-15-1025066-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/ecf0d8c3b43a/fnmol-15-1025066-g0011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/2e42de2a5611/fnmol-15-1025066-g0012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/3f2e017ba3a9/fnmol-15-1025066-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/7e37164a363b/fnmol-15-1025066-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/d5aa184ec988/fnmol-15-1025066-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/8c93a93df9bd/fnmol-15-1025066-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/722374caf230/fnmol-15-1025066-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/e96b95058ae2/fnmol-15-1025066-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/ce277adb715e/fnmol-15-1025066-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/fcafdce34d72/fnmol-15-1025066-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff77/9868638/02247c8410f5/fnmol-15-1025066-g0010.jpg

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[3]
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[4]
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[5]
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[6]
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[10]
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[2]
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Cell Mol Neurobiol. 2025-5-19

[3]
Unravelling the role of protein kinase R (PKR) in neurodegenerative disease: a review.

Mol Biol Rep. 2025-4-9

[4]
Alkaloids as neuroprotectors: targeting signaling pathways in neurodegenerative diseases.

Mol Cell Biochem. 2025-4-7

[5]
Traditional Chinese Medicine-derived formulations and extracts modulating the PI3K/AKT pathway in Alzheimer's disease.

Front Pharmacol. 2025-3-17

[6]
Modulating Neuroinflammation as a Prospective Therapeutic Target in Alzheimer's Disease.

Cells. 2025-1-22

[7]
Evodiamine: A Extremely Potential Drug Development Candidate of Alkaloids from .

Int J Nanomedicine. 2024

[8]
Discovery of FO-4-15, a novel 1,2,4-oxadiazole derivative, ameliorates cognitive impairments in 3×Tg mice by activating the mGluR1/CaMKIIα pathway.

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[9]
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[10]
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本文引用的文献

[1]
Diallyl sulfide protects against dilated cardiomyopathy via inhibition of oxidative stress and apoptosis in mice.

Mol Med Rep. 2021-12

[2]
Insulin and Insulin Resistance in Alzheimer's Disease.

Int J Mol Sci. 2021-9-15

[3]
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Mol Neurodegener. 2021-7-2

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J Prev Alzheimers Dis. 2021

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Int J Mol Sci. 2021-5-19

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CAR-T cell-mediated depletion of immunosuppressive tumor-associated macrophages promotes endogenous antitumor immunity and augments adoptive immunotherapy.

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Neurochem Res. 2021-4

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Brain Pathol. 2020-9

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Evodiamine derivatives improve cognitive abilities in APP/PS1 transgenic mouse models of Alzheimer's disease.

Animal Model Exp Med. 2020-6-29

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