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Published on: February 20, 2019
Screening of Anti-Atherosclerosis Targets of Ce-Bai-Si-Wei Decoction Based on Multidimensional Data and Study on
Wanlu Sheng1, Lina Dai2, Chengyao Wang3
1College of Pharmacy, Inner Mongolia Medical University, Hohhot, China, immu.edu.cn.
Insights
Ce-Bai-Si-Wei decoction (CSD) treats atherosclerosis by targeting key genes like HMOX1 and SELE in macrophages and endothelial cells. CSD reduces inflammation and lipid accumulation, protecting vascular health.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background:
- Atherosclerosis (AS) is a major cause of cardiovascular disease, driven by inflammation, lipid issues, and endothelial damage.
- The therapeutic potential of Ce-Bai-Si-Wei decoction (CSD) for AS is suggested, but its molecular mechanisms require elucidation.
- This study integrates multi-omics and experimental methods to uncover CSD's core molecular pathways in AS.
Purpose of the Study:
- To investigate the molecular mechanisms of Ce-Bai-Si-Wei decoction (CSD) in treating atherosclerosis (AS).
- To identify key molecular targets and pathways affected by CSD in AS.
- To validate the therapeutic effects of CSD on AS using in vitro models and molecular techniques.
Main Methods:
- Network pharmacology was used to predict CSD's active components and targets.
- Microarray and single-cell transcriptomics data were integrated to identify AS regulatory pathways.
- In vitro studies utilized an ox-LDL-induced macrophage foam cell model to assess CSD's effects on lipid accumulation and gene expression.
- Molecular docking, dynamics simulations, RT-qPCR, and Western blot validated CSD's interactions with core targets.
Main Results:
- Four core genes (HMOX1, SELE, CD4, FLT1) were identified as key regulators of inflammation and oxidative stress in AS, interacting with CSD components.
- CSD demonstrated efficacy in reducing ox-LDL-induced lipid accumulation in macrophages and downregulating pro-inflammatory cytokines TNF-α and IL-1β.
- The anti-atherosclerotic effect of CSD was mechanistically linked to the NRF2/HMOX1 pathway, with downregulated FLT1 and SELE in damaged endothelial cells.
- Single-cell analysis indicated CSD primarily targets macrophages and endothelial cells in AS.
Conclusions:
- CSD exerts anti-atherosclerotic effects by modulating core targets HMOX1, SELE, FLT1, and CD4.
- Macrophages and endothelial cells are identified as key effector cells for CSD's action in AS.
- CSD's therapeutic benefits stem from inhibiting inflammation, reducing lipid accumulation, and preserving endothelial function.
Background:
Atherosclerosis (AS), which causes chronic inflammation, aberrant lipid metabolism and vascular endothelial damage, is the main cause of cardiovascular disease. The Ce-Bai-Si-Wei decoction (CSD) may reduce AS, although its molecular mechanisms are unknown. This study investigates core molecular pathways using multi-omics integration and experimental validation.
Method:
Network pharmacology prediction: Construct a 'drug-component-target-disease' interaction network using databases like TCMSP, HIT and ETCM to identify active components and targets of CSD. AS regulatory targets and signalling pathways can be identified by integrating microarray data and single-cell transcriptomics data. In vitro validation: Utilise the OX-LDL-induced model of macrophage foam cells to test CSD's effects on lipid accumulation utilising CCK-8, Oil Red O and TC/TG quantification. Validate CSD's regulatory effects on core targets using molecular docking, molecular dynamics simulation, RT-qPCR and Western blot.
Results:
Four core genes, HMOX1, SELE, CD4 and FLT1, were identified as key regulators of inflammation and oxidative stress in AS, and they bind stably to the active components of CSD. Single-cell data analysis suggested that CSD may improve AS by targeting macrophages and endothelial cells. In vitro, CSD reduced ox-LDL-induced lipid accumulation in macrophages and downregulated TNF-α and IL-1β. Mechanistically, the anti-AS effect of CSD depends on the NRF2/HMOX1 pathway. CSD also downregulated FLT1 and SELE in damaged endothelial cells.
Conclusion:
This study investigated the mechanism of CSD in treating AS. CSD acts on the core targets HMOX1, SELE, FLT1 and CD4, with macrophages and endothelial cells as key effector cells. It exerts anti-AS effects by inhibiting inflammation, reducing lipid accumulation and protecting endothelial function.