ArticleJournal of ginseng research2019
Ginsenoside compound K protects human umbilical vein endothelial cells against oxidized low-density lipoprotein-induced injury via inhibition of nuclear factor-κB, p38, and JNK MAPK pathways.
Article in Journal of ginseng research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Review of OxLDL Driven Inflammatory Cell Activation.Current atherosclerosis reports · 2025Pooled it
- Review
- Autophagy-mediated Kupffer cell polarization in liver cirrhosis reversal: Mechanistic insights and therapeutic strategies.Liver research (Beijing, China) · 2026Review
- Ginsenoside Rg1 promotes skin flap survival by alleviating mitochondrial oxidative stress and apoptosis via the JNK/ERK/p38 pathway.Journal of ginseng research · 2026Article
- Role of natural products in cardiovascular disease.Molecular and cellular biochemistry · 2025Review
- Bu-Yi-Xin-Shen formula targets monocytes through PI3K-Akt/NF-κB signaling in post-percutaneous coronary intervention angina.American journal of translational research · 2025Article
- Anti-Inflammatory Effects of Fermented and Aged Mountain-Cultivated Ginseng Sprouts via Suppression of MAPK-NF-κB Pathway in Lipopolysaccharide-Stimulated RAW264.7 Macrophages.Food science & nutrition · 2024Article
- Article
- Shenfu injection: a review of pharmacological effects on cardiovascular diseases.Frontiers in pharmacology · 2024Review
- A novel dammarane triterpenoid alleviates atherosclerosis by activating the LXRα pathway.Chinese medicine · 2023Article
- m6A-related bioinformatics analysis and functional characterization reveals that METTL3-mediated NPC1L1 mRNA hypermethylation facilitates progression of atherosclerosis via inactivation of the MAPK pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- FoliumPharmaceutical biology · 2022Article
- Advances in the Bioactivities of Phytochemical Saponins in the Prevention and Treatment of Atherosclerosis.Nutrients · 2022Review
- Compound K attenuates hyperglycemia by enhancing glucagon-like peptide-1 secretion through activating TGR5 via the remodeling of gut microbiota and bile acid metabolism.Journal of ginseng research · 2022Article
- A narrative review of the pharmacology of ginsenoside compound K.Annals of translational medicine · 2022Review
- Functional compounds of ginseng and ginseng-containing medicine for treating cardiovascular diseases.Frontiers in pharmacology · 2022Review
- The promising therapeutic potentials of ginsenosides mediated through p38 MAPK signaling inhibition.Heliyon · 2021Review
- Characterization of hyperglycemia due to sub-chronic administration of red ginseng extract via comparative global proteomic analysis.Scientific reports · 2021Article
- Functional roles and mechanisms of ginsenosides from Panax ginseng in atherosclerosis.Journal of ginseng research · 2021Review
- Ginsenoside Compound K: Insights into Recent Studies on Pharmacokinetics and Health-Promoting Activities.Biomolecules · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOxidized low-density lipoprotein (ox-LDL) causes vascular endothelial cell inflammatory response and apoptosis and plays an important role in the development and progression of atherosclerosis. Ginsenoside compound K (CK), a metabolite produced by the hydrolysis of ginsenoside Rb1, possesses strong anti-inflammatory effects. However, whether or not CK protects ox-LDL-damaged endothelial cells and the potential mechanisms have not been elucidated.
methodsIn our study, cell viability was tested using a 3-(4, 5-dimethylthiazol-2yl-)-2,5-diphenyl tetrazolium bromide (MTT) assay. Expression levels of interleukin-6, monocyte chemoattractant protein-1, tumor necrosis factor-α, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 were determined by enzyme-linked immunosorbent assay and Western blotting. Mitochondrial membrane potential (ΔΨm) was detected using JC-1. The cell apoptotic percentage was measured by the Annexin V/ propidium iodide (PI) assay, lactate dehydrogenase, and caspase-3 expression. Apoptosis-related proteins, nuclear factor (NF)-κB, and mitogen-activated protein kinases (MAPK) signaling pathways protein expression were quantified by Western blotting.
resultsOur results demonstrated that CK could ameliorate ox-LDL-induced human umbilical vein endothelial cells (HUVECs) inflammation and apoptosis, NF-κB nuclear translocation, and the phosphorylation of p38 and c-Jun N-terminal kinase (JNK). Moreover, anisomycin, an activator of p38 and JNK, significantly abolished the anti-apoptotic effects of CK.
conclusionThese results demonstrate that CK prevents ox-LDL-induced HUVECs inflammation and apoptosis through inhibiting the NF-κB, p38, and JNK MAPK signaling pathways. Thus, CK is a candidate drug for atherosclerosis treatment.
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