Propolis ameliorates restenosis in hypercholesterolemia rabbits with carotid balloon injury by inhibiting lipid accumulation, oxidative stress, and TLR4/NF‐κB pathway

Ji, Chao; Pan, Yongming; Xu, Songtao; Chen, Yu; Ji, Jian; Chen, Minli; Hu, Fuliang

doi:10.1111/jfbc.13577

Cited by 19 publications

(9 citation statements)

References 38 publications

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“…Similar result was also observed in the hypercholesterolemia rabbits. Propolis consumption reduced the level of C-reactive protein, IL-6, and TNF-α, and inhibited the expression of CD68, TLR4, NF-κB p65, MMP-9, and TNF-α in the carotid arteries [ 73 ]. Further, Cardinault [ 74 ] found that propolis induced the expression of Nrf2-target genes in adipocytes, transactivated Nrf2 response element and the Nrf2 DNA-binding in mice [ 74 ].…”

Section: Resultsmentioning

confidence: 99%

Recent Update on the Anti-Inflammatory Activities of Propolis

et al. 2022

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In recent years, research has demonstrated the efficacy propolis as a potential raw material for pharmaceuticals and nutraceuticals. There is limited report detailing the mechanisms of action of propolis and its bioactive compounds in relation to their anti-inflammatory properties. Thus, the aim of the present review is to examine the latest experimental evidence (2017–2022) regarding the anti-inflammatory properties of propolis. A systematic scoping review methodology was implemented. After applying the exclusion criteria, a total of 166 research publications were identified and retrieved from Scopus, Web of Science, and Pubmed. Several key themes related to the anti-inflammatory properties of propolis were subsequently identified, namely in relation to cancers, oral health, metabolic syndrome, organ toxicity and inflammation, immune system, wound healing, and pathogenic infections. Based on the latest experimental evidence, propolis is demonstrated to possess various mechanisms of action in modulating inflammation towards the regulatory balance and anti-inflammatory environment. In general, we summarize that propolis acts as an anti-inflammatory substance by inhibiting and downregulating TLR4, MyD88, IRAK4, TRIF, NLRP inflammasomes, NF-κB, and their associated pro-inflammatory cytokines such as IL-1β, IL-6, IFN-γ, and TNF-α. Propolis also reduces the migration of immune cells such as macrophages and neutrophils, possibly by downregulating the chemokines CXCL9 and CXCL10.

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Section: Resultsmentioning

confidence: 99%

Recent Update on the Anti-Inflammatory Activities of Propolis

et al. 2022

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“…STAT1 [493], JAK2 [494], NOTCH2 [495], PDGFC (platelet derived growth factor C) [143], RASA1 [262], TLR6 [496], NOD2 [482], JMJD1C [483], CAVIN1 [485], POU2F1 [497], RPS5 [498] and LGALS3 [499] are involved in the regulation of cardiac fibrosis. TLR4 [500], ABCA1 [501], CCR2 [502], LDLR (low density lipoprotein receptor) [503], SIRT1 [504] and NOD2 [505] might crucially contribute to the development of hypercholesterolemia. ABCA1 [506], TLR5 [507], PTGS2 [508], TGFA (transforming growth factor alpha) [509], PDK4 [510], JAK2 [511], TLR2 [512], NEK7 [513], CCR1 [514], BACH1 [515], NCOA4 [195], LATS2 [516], PELI1 [517], EGR1 [518], CYBB (cytochrome b-245 beta chain) [519], MEFV (MEFV innate immuity regulator, pyrin) [520], CLEC4E [521], GCLC (glutamate-cysteine ligase catalytic subunit) [522], KLF3 [523], TP53INP1 [524], ITGB1 [525], IRF9 [526], PHLPP1 [527], NOD2 [528], ACSL4 [529], FGL2 [530], PF4 [531], VEGFB (vascular endothelial growth factor B) [532], CCR7 [533], IGFBP4 [534], TRPM4 [535], BAG1 [536], LGALS3 [537] and ATAD3A [538] could induce ischemic heart disease.…”

Section: Discussionmentioning

confidence: 99%

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Vastrad¹,

Vastrad²

2023

Preprint

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Coronary artery disease (CAD) is the most common cardiovascular disorder and the leading cause of heart related deaths in world. Increasing molecular targets have been discovered for CAD and CAD - related complications prognosis and therapy. However, there is still an urgent need to identify novel biomarkers. Therefore, we evaluated biomarkers that might help the diagnosis and treatment of CAD and CAD related complications. We searched next generation sequencing (NGS) dataset (GSE202625) and identified differentially expressed genes (DEGs) by comparing CAD and normal control samples using DESeq2. Gene ontology (GO) and pathway enrichment analyses of the DEGs were performed using the g:Profiler online database. The protein protein interaction (PPI) network was plotted with IMEx interactome and visualized using Cytoscape. Module analysis of the PPI network was done using PEWCC1. MiRNA hub gene regulatory network and TF hub gene regulatory network analysis was performed to identify the hub genes, miRNAs and TFs. Receiver operating characteristic (ROC) curve analysis was used to predict the diagnostic effectiveness of the hub genes. A total of 118 DEGs (479 up regulated genes and 479 down regulated genes) were detected. The GO enrichment analysis indicated that the DEGs most significantly enriched in cellular response to stimulus and biosynthetic process. The REACTOME pathway enrichment analysis revealed that the DEGs were most significantly enriched in immune system and eukaryotic translation elongation. PPI network, modules, miRNA hub gene regulatory network and TF hub gene regulatory network analysis demonstrated that EGR1, SIRT1, STAT1, LRRK2, HIF1A, CSNK2B, RPS3, RPS2, RPS4X and HDAC11 were the hub genes. On the whole, the findings of this study enhance our understanding of the potential molecular mechanisms of CAD and CAD-related complications, and provide potential targets for further research.

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“…Furthermore, attenuating oxidative stress may potentially decelerate the progression of atherosclerotic plaque formation ( 22 ). Ji et al ( 23 ) revealed that propolis ameliorated restenosis in hypercholesterolemia rabbits with carotid balloon injury by inhibiting lipid accumulation, oxidative stress and the Toll-like receptor 4/NF-κB signaling pathway. Zhang et al ( 24 ) reported that quercetin is a potential therapeutic agent ameliorating atherosclerotic pathophysiology in rat carotid arteries by inhibiting oxidative stress and inflammatory response, the mechanism of which involved modulating the AMP-activated protein kinase/sirtuin 1/NF-κB signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Identification of pathways and key genes in male late‑stage carotid atherosclerosis using bioinformatics analysis

Zhang

Jing

et al. 2022

Exp Ther Med

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Late-stage carotid atherosclerosis has a high incidence rate and may lead to various cerebrovascular diseases. The gene expression profile GSE100927 was selected to identify differentially expressed genes (DEGs) in carotid atherosclerosis. Subsequently, protein-protein interaction, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were conducted. Furthermore, experimental verification was performed using human umbilical vein endothelial cells (HUVECs), human aortic vascular smooth muscle cells (HAVSMCs) and Tohoku Hospital Pediatrics-1 (THP-1)-induced macrophages. The groups were as follows: Control group, solvent control group and palmitic acid group. The levels of reactive oxygen species (ROS) in the three cell types were detected by flow cytometry or fluorescence microscopy. Furthermore, apoptosis of HUVECs and HAVSMCs was assessed by flow cytometry and the nuclear Hoechst 33258 staining of THP-1-induced macrophages was performed. Male late-stage carotid atherosclerosis samples, including 10 control samples and 21 atherosclerosis samples, were selected. Pathway enrichment analysis demonstrated that ‘Toll-like receptor signaling pathway’ was the top pathway associated with the DEGs. MMP7, MMP9, IL1β, C-C motif chemokine ligand 4 (CCL4), secreted phosphoprotein 1 (SPP1), CCL3 and interferon regulatory factor 5 (IRF5) were selected for experimental verification. Palmitic acid increased the ROS levels and the apoptosis rates of HUVECs and HAVSMCs. However, it did not increase the levels of ROS and did not shrink the nuclei of THP-1-induced macrophages. Furthermore, palmitic acid increased the mRNA levels of IL1β, CCL4, SPP1, CCL3, IRF5, MMP7 and MMP9 in HUVECs and THP-1-induced macrophages, and increased the mRNA levels of CCL4 and MMP9 in HAVSMCs. In conclusion, IL1β, CCL3, CCL4, SPP1, IRF5, MMP7 and MMP9 are important markers of late-stage carotid atherosclerosis.

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Propolis ameliorates restenosis in hypercholesterolemia rabbits with carotid balloon injury by inhibiting lipid accumulation, oxidative stress, and TLR4/NF‐κB pathway

Cited by 19 publications

References 38 publications

Recent Update on the Anti-Inflammatory Activities of Propolis

Recent Update on the Anti-Inflammatory Activities of Propolis

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Identification of pathways and key genes in male late‑stage carotid atherosclerosis using bioinformatics analysis

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