Mechanism of albiflorin in improvement of Alzheimer's disease based on network pharmacology and in vitro experiments.
10.19540/j.cnki.cjcmm.20230510.701
- Author:
Hui XUE
1
;
Jing JIANG
2
;
Yue ZHANG
2
;
Xue-Tong MENG
2
;
Ao XUE
2
;
Yue QIAO
2
;
Xia LEI
3
;
Ji-Hui ZHAO
4
;
Ning ZHANG
2
Author Information
1. School of Pharmacy, Heilongjiang University of Chinese Medicine Harbin 150040, China College of Jiamusi, Heilongjiang University of Chinese Medicine Jiamusi 154007, China.
2. School of Pharmacy, Heilongjiang University of Chinese Medicine Harbin 150040, China.
3. Wuxi Traditional Chinese Medicine Hospital Wuxi 214071, China.
4. School of Pharmaceutical Sciences, Hunan University of Medicine Huaihua 418000, China.
- Publication Type:Journal Article
- Keywords:
Alzheimer′s disease;
ERK1/2;
MAPK/ERK;
albiflorin;
molecular docking;
network pharmacology
- MeSH:
Animals;
Rats;
Alzheimer Disease/drug therapy*;
bcl-2-Associated X Protein;
Network Pharmacology;
Molecular Docking Simulation
- From:
China Journal of Chinese Materia Medica
2023;48(17):4738-4746
- CountryChina
- Language:Chinese
-
Abstract:
This study aimed to explore the mechanism of albiflorin in the treatment of Alzheimer's disease(AD) based on network pharmacology, molecular docking, and in vitro experiments. Network pharmacology was used to predict the potential targets and pathways of albiflorin against AD, and molecular docking technology was used to verify the binding affinity of albiflorin to key target proteins. Finally, the AD cell model was induced by Aβ_(25-35) in rat pheochromocytoma(PC12) cells and intervened by albiflorin to validate core targets and pathways. The results of network pharmacological analysis showed that albiflorin acted on key targets such as mitogen-activated protein kinase-1(MAPK1 or ERK2), albumin(ALB), epidermal growth factor receptor(EGFR), caspase-3(CASP3), and sodium-dependent serotonin transporter(SLC6A4), and signaling pathways such as MAPK, cAMP, and cGMP-PKG. The results of molecular docking showed that albiflorin had strong binding affinity to MAPK1(ERK2). In vitro experiments showed that compared with the blank group, the model group showed decreased cell viability, decreased expression level of B-cell lymphoma 2(Bcl-2), increased Bcl-2-associated X protein(Bax), and reduced phosphorylation level of extracellular signal-regulated kinase 1/2(ERK1/2) and the relative expression ratio of p-ERK1/2 to ERK1/2. Compared with the model group, the albiflorin group showed potentiated cell viability, up-regulated expression of Bcl-2, down-regulated Bax, and increased phosphorylation level of ERK1/2 and the relative expression ratio of p-ERK1/2 to ERK1/2. These results suggest that the mechanism of albiflorin against AD may be related to its activation of the MAPK/ERK signaling pathway and its inhibition of neuronal apoptosis.
