Mechanism of Acanthopanacis Senticosi Radix et Rhizoma seu Caulis Extract in Treating Parkinson's Disease Based on Lipidomics
10.13422/j.cnki.syfjx.20250714
- VernacularTitle:基于脂质组学探讨刺五加提取物治疗帕金森小鼠的作用机制
- Author:
Ningxia LU
1
;
Ao GAO
1
;
Yehao WANG
1
;
Jinjin YANG
1
;
Yi LU
2
;
Fang LU
3
;
Shumin LIU
3
Author Information
1. Graduate School，Heilongjiang University of Chinese Medicine，Harbin 150040，China
2. Key Laboratory of Modern Chinese Medicine Preparation of Ministry of Education， Jiangxi University of Traditional Chinese Medicine， Nanchang 330004， China
3. Institute of TCM，Heilongjiang University of Chinese Medicine，Harbin 150040，China
- Publication Type:Journal Article
- Keywords:
Acanthopanacis Senticosi Radix et Rhizoma seu Caulis extract;
Parkinson's disease;
lipidomics;
network pharmacology
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(6):91-99
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveAbnormal lipids in neurons can cause the accumulation of α-synuclein（α-syn）. This study aimed to explore the mechanism of Acanthopanacis Senticosi Radix et Rhizoma seu Caulis extract （ASH） in treating Parkinson's disease （PD） mice using lipidomics combined with network pharmacology. MethodsMice were divided into the blank group， model group and ASH （45.5 mg·kg-1） group. Motor ability was evaluated by pole climbing time and autonomous activity count； The oxidative stress indicators were detected by enzyme-linked immunosorbent assay （ELISA）. Lipid biomarkers in brain tissues were screened and identified by ultra-performance liquid chromatography-tandem mass spectrometry （UPLC-MS/MS）， and metabolic pathway analysis was conducted. The key targets of ASH for PD treatment were explored using network pharmacology. The Kyoto Encyclopedia of Genes and Genomes （KEGG） database was used for pathway enrichment analysis， and the "compound-reaction-enzyme-gene" network was constructed using the MetScape plugin. The protein expression levels of glutathione S-transferase P1 （GSTP1）， glutathione S-transferase Mu 2 （GSTM2）， prostaglandin peroxide synthase 1 （PTGS1）， prostaglandin peroxide synthase 2 （PTGS2）， and prostaglandin E synthase （PTGES） were validated by Western blot. ResultsCompared with the blank group， the model group showed significantly prolonged pole climbing time and reduced autonomous activity count （P<0.01）. Compared with the model group， the ASH group demonstrated significantly faster pole climbing and increased autonomous activity count （P<0.01）. The model group exhibited significantly decreased superoxide dismutase （SOD） and glutathione peroxidase （GSH-Px） levels， and increased malondialdehyde （MDA） level in brain tissues compared with the blank group （P<0.01）. The ASH group showed increased SOD and GSH-Px levels and decreased MDA level compared with the model group （P<0.05， P<0.01）. Lipidomics analysis identified 10 differential metabolites and 8 differential metabolic pathways. Network pharmacological analysis revealed 213 intersection targets between ASH components and PD， with KEGG enrichment involving the sphingolipid signaling pathway， lipid arteriosclerosis， phosphoinositide 3-kinase/protein kinase B（PI3K/Akt） signaling pathway， mitogen-activated protein kinase（MAPK） signaling pathway， and hypoxia inducible factor-1（HIF-1） signaling pathway. Integrated lipidomics and network pharmacology analysis highlighted the central role of the arachidonic acid metabolic pathway. The Western blot results showed that ASH effectively up-regulated GSTP1， GSTM2， and PTGS1 protein expression， and down-regulated PTGS2 and PTGES protein expression. ConclusionASH can ameliorate behavioral deficits， exert antioxidant effects， regulate lipid differential metabolites and the arachidonic acid metabolic pathway， thereby exerting therapeutic effects in PD model mice.
