Mechanism of salidroside against coronary artery disease by network pharmacology analysis

Tao, Lin; Liang, Zhi-Fang; Miao, Liu; Guo, Yu-Jie; Li, Ye; Liu, Yan-Li; Fang, Dong-Ming; Yang, Zhi-Jie

doi:10.1186/s12906-023-04027-3

Mechanism of salidroside against coronary artery disease by network pharmacology analysis

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Published: 12 June 2023

Volume 23, article number 194, (2023)
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Mechanism of salidroside against coronary artery disease by network pharmacology analysis

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Lin Tao¹^na1,
Zhi-Fang Liang¹^na1,
Liu Miao¹,
Yu-Jie Guo¹,
Ye Li¹,
Yan-Li Liu¹,
Dong-Ming Fang¹ &
…
Zhi-Jie Yang¹

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Abstract

Background

Rosenroot (Rhodiola rosea) is a traditional Chinese herbal medicine. It has been used to treat patients with coronary artery disease (CAD). Salidroside is the main active constituent of rosenroot. This study was designed to explore the mechanism of salidroside in treating CAD and its role in angiogenesis in CAD systematically.

Methods

In this study, potential targets related to salidroside and CAD were obtained from public databases. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Disease Ontology (DO) and CellMarker enrichment analyses were performed. The binding of salidroside to angiogenesis-related targets was assessed by PyMOL and Ligplot. Furthermore, the effects of salidroside on collateral circulation were evaluated by correlation analysis of these angiogenesis-related targets with the coronary flow index (CFI), and the influence of salidroside on human umbilical vein endothelial cell (HUVEC) proliferation and migration was assessed.

Results

Eighty-three targets intersected between targets of salidroside and CAD. GO and KEGG analyses indicated that salidroside mainly treated CAD through angiogenesis and anti-inflammatory action. There were 12 angiogenesis-related targets of salidroside in coronary heart disease, among which FGF1 (r = 0.237, P = 2.597E-3), KDR (r = 0.172, P = 3.007E-2) and HIF1A (r = -0.211, P = 7.437E-3) were correlated with the coronary flow index (CFI), and salidroside docked well with them. Finally, cell experiments confirmed that salidroside promoted the proliferation and migration of HUVECs.

Conclusions

This study revealed the potential molecular mechanism of salidroside on angiogenesis in CAD and provided new ideas for the clinical application of salidroside in the treatment of CAD.

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Background

Coronary artery disease (CAD), also known as coronary atherosclerotic heart disease, is a principal cause of cardiovascular death globally, and the mortality rates of CAD are increasing annually [1]. Percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) have greatly improved the symptoms and prognosis of CAD. However, certain patients cannot be treated surgically because of diffuse coronary artery disease [2]. Currently, effective angiogenesis and coronary collateral circulation are critical as they curtail cardiovascular events and ameliorate prognosis [3, 4].

Rosenroot (Rhodiola rosea) is a traditional Chinese herbal medicine and has significant medicinal and health benefits [5]. It has been extensively employed for numerous diseases, such as coronary artery diseases, hypertension, heart failure, heart arrhythmia and other cardiovascular diseases [6, 7]. Salidroside, one of the key active constituents of rosenroot, has been synthesized for clinical treatment and basic research. It plays an important role in the cardiovascular system due to its anti-hypoxia and antioxidant activities, antiaging activities, anti-inflammatory and antidiabetic activities [Full size image

Enrichment analysis of salidroside-related targets and targets for treatment of CAD

Through the Metascape online analysis tool, many GO terms and KEGG terms related to salidroside-related targets and targets for the treatment of CAD were enriched (Fig. 5), and the PPI network and key modules between the targets were obtained (Fig. 6). Interestingly, both salidroside-related targets and targets for the treatment of CAD were enriched in the biological processes of epithelial cell proliferation and morphogenesis of the epithelium. In addition to key module analysis results, there was still a high correlation with epithelial cell proliferation (Table 2). Further CellMarker enrichment and disease ontology analyses were performed by R (Fig. 5). The detailed results can be found in Supplementary Table 2. Notably, CellMarker enrichment analysis of the targets for the treatment of CAD revealed that these targets were enriched in blood vessels, bone marrow, muscle and other normal tissues. It was also enriched in endothelial cells and endothelial progenitor cells.

Table 2 Top 3 biological processes of Top 3 modules between targets of salidroside and targets of salidroside in the treatment of CAD

Full size table

Salidroside and angiogenesis

Twenty-five gene sets related to angiogenesis were found in misgdb, containing a total of 463 genes (Supplementary Table 3). After intersecting the angiogenesis-related genes and the target of salidroside in the treatment of CAD, 12 genes remained, including VEGFA, KDR, CD34, FGF2, AKT1, FGF1, IL10, TEK, CCND2, IL32, HLA-C, and HIF1A. To further evaluate the binding affinity of these targets and salidroside, molecular docking analysis was conducted. However, the protein structures of CD34 and IL32 were not found in the Protein Data Bank, so they were excluded. The binding energies of salidroside and target proteins are shown in Table 3. The results showed that the docking energy of salidroside with the protein receptor ranged from -3.8 kcal/mol to -8.4 kcal/mol. These results suggested that salidroside docked well with these angiogenesis-related proteins under natural conditions. In particular, salidroside presented the lowest docking energy with AKT1 (docking energy: -8.4 kcal/mol). Furthermore, the correlation analysis showed that CFI was positively correlated with FGF1 (r = 0.237, P = 2.597E-3) and KDR (r = 0.172, P = 3.007E-2) but negatively correlated with HIF1A (r = -0.211, P = 7.437E-3). The detailed results are shown in Fig. 7. Finally, molecular docking results of salidroside with FGF1, KDR and HIF1A were visualized using pyMOL and Ligplot (Fig. 8). Salidroside mainly binds to the targets by forming multiple hydrogen bonds and hydrophobic interactions with the amino acid residues.

Table 3 The docking scores of salidroside with angiogenesis-related proteins

Full size table

Salidroside promotes the proliferation and migration of HUVECs

To verify the effect of salidroside on HUVECs, CCK-8 and wound healing assays were performed. Our results indicated that 30 μM salidroside significantly increased the capacity to proliferate and migrate HUVECs compared with the control group (P < 0.01, Fig. 9). These results suggested that salidroside enhanced endothelial cell proliferation and migration and angiogenesis.

Discussion

The pathophysiological mechanisms of CAD are complex. It is well known that CAD is a chronic inflammatory disease. Several proinflammatory cytokines, such as IL-6, IL-18, TNF-α and C-reactive protein, have been reported to be independently associated with the risk of coronary heart disease [24, 25]. In atherosclerotic lesions, inflammatory cells such as T cells, macrophages and mast cells release various inflammatory cytokines and proteolytic enzymes. Phenotypic transformation of vascular smooth muscle cells (VSMCs) is then induced, leading to the proliferation and migration of VSMCs and ultimately promoting the progression of atherosclerotic lesions [26]. Thus, some clinical trials have also demonstrated that anti-inflammatory agents such as colchicine and interleukin-1β antagonists can reduce cardiovascular events and decrease mortality in patients with CAD [27, 28]. In addition to the inflammatory response, oxidative stress, hypoxia and other mechanisms promote the occurrence and development of CAD synergistically.

The enrichment analysis of salidroside in the treatment of CAD suggests that salidroside can regulate inflammatory biological processes, such as leukocyte apoptotic process, leukocyte migration, and inflammatory response in the treatment of CAD, which is consistent with the pharmacological mechanism of salidroside [8]. Salidroside may inhibit the formation of ox-LDL-induced THP1-derived foam cells by inhibiting oxidative stress and the inflammatory response, thus playing an antiatherosclerotic role [29]. In addition, salidroside has a protective effect on myocardial injury in coronary artery occlusion-induced rats by regulating AMPK-related signaling cascades and inhibiting excessive release of myocardial enzymes and proinflammatory cytokines [30].

More intriguingly, many biological processes and signaling pathways related to angiogenesis were enriched in the enrichment analysis. Angiogenesis is the formation of new blood vessels. In the process of angiogenesis, endothelial cells proliferate, migrate and assemble to form tubular structures and then recruit smooth muscle cells and parietal cells to form mature blood vessels [31, 32]. High angiogenic capacity can promote the formation of coronary artery collateral branches, which improves cardiac circulation and myocardial contractility and reduces the incidence of adverse vascular events and mortality. Heeschen et al. reported that angiogenesis-related factors vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) are independent prognostic factors in patients with acute coronary syndrome, and HGF elevation is associated with improved collateralization [33]. Secretoneurin has been reported to increase VEGF-induced VEGFR2 activation and VEGF binding to human coronary artery endothelial cells (HCAECs) and induce the infarct border zone of coronary angiogenesis in a rat model of myocardial infarction [34]. Many clinical trials have shown that VEGF-based angiogenesis therapy can improve cardiac perfusion and angina class compared with placebo [35, 36]. Despite the great promise of angiogenesis gene therapy, previous studies have limited efficacy. Current randomized controlled trials have not met promising results [37]. This may be due to the low dose of agents in the local tissue of the heart and the composition of the single agent.

Actually, salidroside has been shown to promote angiogenesis significantly. It has been.reported that salidroside can increase the expression of VEGF and NO, thus promoting the angiogenesis mediated by bone marrow-derived endothelial progenitor cells [38]. Salidroside upregulates HIF-1α expression and enhances its transcriptional activity to VEGF, thereby upregulating VEGF expression at the mRNA and protein levels and finally enhancing angiogenesis and bone formation [39]. In addition, salidroside can increase the microvessels in the infarction boundary area, reduce the area of myocardial infarction and improve cardiac function in myocardial infarction mice [40]. Our molecular docking results showed that salidroside bound to several angiogenic-related factors, among which VEGF, HIF1A and KDR were correlated with coronary artery collateral circulation. In addition, cell experiments also confirmed that salidroside can promote the proliferation and migration of HUVECs. In conclusion, we believe that salidroside plays an important role in angiogenesis and collateral circulation in CAD. Due to the limited efficacy of proangiogenic therapy, salidroside as a complementary therapy may play a synergistic role in promoting angiogenesis in CAD.

Our study also has some limitations. First, we only tested the effect of salidroside on the proliferation and migration of HUVECs, even though some literatures also adopted the same method [41, 42]. However, the effect of salidroside on coronary collateral formation needs to be further verified by coronary endothelial cells and in vivo experiments. Second, even if the potential target of salidroside in promoting angiogenesis was found in this study, PCR or Western blot or surface plasmon resonance technology should be used to further verify the results in the follow-up study.

Conclusions

Overall, in this study, the pharmacological mechanism of salidroside in CAD was investigated using network pharmacology and experimental methods. Salidroside may improves angiogenesis and collateral circulation in patients with CAD by regulating VEGF, HIF1A and KDR and other angiogenesis-related factors. However, the final mechanism needs to be further verified by subsequent experiments.

Availability of data and materials

The datasets generated and/or analysed during the current study are publicly available. The database links used in this article are as follows: PubChem database (https://pubchem.ncbi.nlm.nih.gov/), TCMSP database (https://tcmsp-e.com/), the Encyclopedia of Traditional Chinese Medicine (ETCM, http://www.tcmip.cn/ETCM/), similarity ensemble approach (SEA, https://sea.bkslab.org/), STITCH database (http://stitch.embl.de/), Gene Expression Omnibus database (GEO, https://www.ncbi.nlm.nih.gov/geo/), DisGeNET (https://www.disgenet.org/), DrugBank (https://www.drugbank.com/), GeneCards (https://www.genecards.org/), The Human Phenotype Ontology (HPO, https://hpo.jax.org/app/), NCBI-gene (https://www.ncbi.nlm.nih.gov/gene/), Online Mendelian Inheritance in Man (OMIM, https://omim.org/), PharmGKB (https://www.pharmgkb.org/), The CellMarker database (http://xteam.xbio.top/CellMarker/), Molecular Signatures Database (MSigDB, https://www.gsea-msigdb.org/gsea/msigdb), Protein Data Bank (http://www.rcsb.org/pdb/), and Metascape (https://metascape.org).

Abbreviations

CAD:: Coronary artery disease
GO:: Gene ontology
KEGG:: Kyoto encyclopedia of genes and genomes
DO:: Disease ontology
CFI:: Coronary flow index
HUVEC:: Human umbilical vein endothelial cell
PCI:: Percutaneous coronary intervention
CABG:: Coronary artery bypass grafting
OB:: Oral bioavailability
Caco-2:: Caco-2 permeability
BBB:: Blood–brain barrier
UniProt:: Universal protein resource
PPI:: Protein–protein interaction
MSigDB:: Molecular signatures database
OD:: Optical density
VSMCs:: Vascular smooth muscle cells
VEGF:: Vascular endothelial growth factor

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Acknowledgements

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Funding

The authors acknowledge the essential role of the funding of National Natural Science Foundation of China (NSFC: 82060072 and 81760073), National Natural Science Foundation of Guangxi (2020GXNSFAA297003), Guangxi Medical High-level Backbone Talent Program (G201903047), Project of Liuzhou Science and Technology (2020NBAB0818), Guangxi self-financing research projects(Z20190137, Z20190738, Z20200460, Z20210480 and Z20210459), the project of Liuzhou people's Hospital (LYRGCC202107) and Guangxi Medical and health key discipline construction project and Guangxi Health Commission Key Laboratory of Clinical Biotechnology (Liuzhou People's Hospital).

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Lin Tao and Zhi-Fang Liang contributed equally to this work.

Authors and Affiliations

Departments of Cardiology, Liuzhou People’s Hospital, 8 Wenchang Road, Liuzhou, 545006, Guangxi, People’s Republic of China
Lin Tao, Zhi-Fang Liang, Liu Miao, Yu-Jie Guo, Ye Li, Yan-Li Liu, Dong-Ming Fang & Zhi-Jie Yang

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Lin Tao
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Zhi-Fang Liang
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Liu Miao
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Yu-Jie Guo
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Ye Li
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Yan-Li Liu
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Contributions

L.T., Y. L and Z.-F.L. participated in the design, and completed the cell experiments. Z.-J.Y. performed the statistical analyses, and drafted the manuscript. D.-M.F. and Y.-J.G. drafted the paper. L.M. and Y.-L.L. designed the project and revised the paper. All authors read and approved the final manuscript.

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Correspondence to Zhi-Jie Yang.

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Supplementary Information

Additional file 1:

Supplementary Table 1. Targets of salidroside, CAD, and salidroside in the treatment of CAD.

Additional file 2:

Supplementary Table 2. Enrichment analysis of salidroside-related targets and targets for treatment of CAD.

Additional file 3:

Supplementary Table 3. Twenty-five gene sets and genes related to angiogenesis in MSigDB.

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Tao, L., Liang, ZF., Miao, L. et al. Mechanism of salidroside against coronary artery disease by network pharmacology analysis. BMC Complement Med Ther 23, 194 (2023). https://doi.org/10.1186/s12906-023-04027-3

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Received: 09 November 2022
Accepted: 06 June 2023
Published: 12 June 2023
DOI: https://doi.org/10.1186/s12906-023-04027-3

Mechanism of salidroside against coronary artery disease by network pharmacology analysis