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Cell Signaling Technology Inc pfkfb3

Re inhibits glycolysis in mice. (A) Representative image of <t>PFKFB3</t> expression in mouse aortic root detected by immunohistochemistry (IHC), n = 3, bar = 100 μm. (B) PFKFB3, HIF-1α, and HK2 mRNA levels in the aorta, n = 3. (C) Western blotting assay and quantitative data of HIF-1α, HK2, and PFKFB3 in aorta, n = 3. ### p < 0.001, ## p < 0.01, # p < 0.05, vs. control group, ∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05 vs. AS group.

Pfkfb3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pfkfb3/pmc12959289-84-9-12?v=Cell+Signaling+Technology+Inc
Average 86 stars, based on 1 article reviews

pfkfb3 - by Bioz Stars, 2026-07

86/100 stars

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1) Product Images from "Ginsenoside Re regulates PFKFB3-mediated glycolysis to inhibit endothelial cell migration to ameliorate atherosclerosis"

Article Title: Ginsenoside Re regulates PFKFB3-mediated glycolysis to inhibit endothelial cell migration to ameliorate atherosclerosis

Journal: Journal of Ginseng Research

doi: 10.1016/j.jgr.2025.11.012

Re inhibits glycolysis in mice. (A) Representative image of PFKFB3 expression in mouse aortic root detected by immunohistochemistry (IHC), n = 3, bar = 100 μm. (B) PFKFB3, HIF-1α, and HK2 mRNA levels in the aorta, n = 3. (C) Western blotting assay and quantitative data of HIF-1α, HK2, and PFKFB3 in aorta, n = 3. ### p < 0.001, ## p < 0.01, # p < 0.05, vs. control group, ∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05 vs. AS group.

Figure Legend Snippet: Re inhibits glycolysis in mice. (A) Representative image of PFKFB3 expression in mouse aortic root detected by immunohistochemistry (IHC), n = 3, bar = 100 μm. (B) PFKFB3, HIF-1α, and HK2 mRNA levels in the aorta, n = 3. (C) Western blotting assay and quantitative data of HIF-1α, HK2, and PFKFB3 in aorta, n = 3. ### p < 0.001, ## p < 0.01, # p < 0.05, vs. control group, ∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05 vs. AS group.

Techniques Used: Expressing, Immunohistochemistry, Western Blot, Control

Re inhibits ox-LDL-induced glycolysis of HUVECs. (A) Glucose uptake by HUVECs, n = 3. (B) Lactate efflux by HUVECs, n = 3. (C) mRNA expression of PFKFB3, HIF-1α, and HK2 in HUVECs, n = 3. (D) Structural formula of ginsenoside Re. (E–G) Predicted binding sites of Re to PFKFB3, HIF-1α, and HK2 by molecular docking. ### p < 0.001, ## p < 0.01, # p < 0.05, vs. control group; ∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05, vs. ox-LDL group.

Figure Legend Snippet: Re inhibits ox-LDL-induced glycolysis of HUVECs. (A) Glucose uptake by HUVECs, n = 3. (B) Lactate efflux by HUVECs, n = 3. (C) mRNA expression of PFKFB3, HIF-1α, and HK2 in HUVECs, n = 3. (D) Structural formula of ginsenoside Re. (E–G) Predicted binding sites of Re to PFKFB3, HIF-1α, and HK2 by molecular docking. ### p < 0.001, ## p < 0.01, # p < 0.05, vs. control group; ∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05, vs. ox-LDL group.

Techniques Used: Expressing, Binding Assay, Control

Re inhibits endothelial cell migration via the PFKFB3-HIF-1α/VEGFA-VEGFR2 signaling pathways. (A) Western blot assay and quantitative analysis of PFKFB3 in HUVECs, n = 3. (B) Cell viability of PFKFB3 overexpressing ECs measured by CCK-8 assay, n = 6. (C) Western blot assay and quantitative analysis of PFKFB3 in HUVECs, n = 3. (D–E) Representative images of HUVEC induced by ox-LDL for 0 h and 12 h in wound healing experiments (bar = 50 μm) and quantification of EC migration, n = 3. (F, G) Western blot assay and quantitative data of VE-cadherin, HIF-1α, VEGFA, and VEGFR2 in HUVECs, n = 3. ### p < 0.001, ## p < 0.01, # p < 0.05, vs. control group; ∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05, vs. ox-LDL group.

Figure Legend Snippet: Re inhibits endothelial cell migration via the PFKFB3-HIF-1α/VEGFA-VEGFR2 signaling pathways. (A) Western blot assay and quantitative analysis of PFKFB3 in HUVECs, n = 3. (B) Cell viability of PFKFB3 overexpressing ECs measured by CCK-8 assay, n = 6. (C) Western blot assay and quantitative analysis of PFKFB3 in HUVECs, n = 3. (D–E) Representative images of HUVEC induced by ox-LDL for 0 h and 12 h in wound healing experiments (bar = 50 μm) and quantification of EC migration, n = 3. (F, G) Western blot assay and quantitative data of VE-cadherin, HIF-1α, VEGFA, and VEGFR2 in HUVECs, n = 3. ### p < 0.001, ## p < 0.01, # p < 0.05, vs. control group; ∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05, vs. ox-LDL group.

Techniques Used: Migration, Protein-Protein interactions, Western Blot, CCK-8 Assay, Control

Image Search Results

Network pharmacology analysis of the PFKFB3 inhibitor 3PO’s potential anti-asthma targets. (A) The chemical structure of 3PO. (B) Venn diagram illustrating 43 overlapping targets between 3PO-predicted targets and asthma-related genes. (C) PPI network constructed from the 43 intersecting targets. (D) Top 9 hub genes identified and visualized in Cytoscape based on degree centrality: node color intensity (red) corresponds to higher connectivity. (E) GO enrichment analysis results, including BP, CC, and MF. (F) KEGG enrichment analysis results. Protein-protein interaction = PPI, GO = Gene ontology, BP = Biological process, CC = Cellular component, MF = Molecular function, KEGG = Kyoto encyclopedia of genes and genomes.

Journal: Frontiers in Pharmacology

Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments

doi: 10.3389/fphar.2026.1790273

Figure Lengend Snippet: Network pharmacology analysis of the PFKFB3 inhibitor 3PO’s potential anti-asthma targets. (A) The chemical structure of 3PO. (B) Venn diagram illustrating 43 overlapping targets between 3PO-predicted targets and asthma-related genes. (C) PPI network constructed from the 43 intersecting targets. (D) Top 9 hub genes identified and visualized in Cytoscape based on degree centrality: node color intensity (red) corresponds to higher connectivity. (E) GO enrichment analysis results, including BP, CC, and MF. (F) KEGG enrichment analysis results. Protein-protein interaction = PPI, GO = Gene ontology, BP = Biological process, CC = Cellular component, MF = Molecular function, KEGG = Kyoto encyclopedia of genes and genomes.

Article Snippet: The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

Techniques: Construct

Molecular docking results of 3PO with the top eight core targets. (A) Molecular docking of 3PO with IL-1β. (B) Molecular docking of 3PO with IL-6. (C) Molecular docking of 3PO with TNF-α. (D) Molecular docking of 3PO with NF-κB p65. (E) Molecular docking of 3PO with Bcl-2. (F) Molecular docking of 3PO with Caspase3. (G) Molecular docking of 3PO with Tau. (H) Molecular docking of 3PO with MAO-B. IL-1β = Interleukin-1β, IL-6 = Interleukin-6, TNF-α = Tumor necrosis factor-α, NF-κB = Nuclear factor kappa B.

Journal: Frontiers in Pharmacology

Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments

doi: 10.3389/fphar.2026.1790273

Figure Lengend Snippet: Molecular docking results of 3PO with the top eight core targets. (A) Molecular docking of 3PO with IL-1β. (B) Molecular docking of 3PO with IL-6. (C) Molecular docking of 3PO with TNF-α. (D) Molecular docking of 3PO with NF-κB p65. (E) Molecular docking of 3PO with Bcl-2. (F) Molecular docking of 3PO with Caspase3. (G) Molecular docking of 3PO with Tau. (H) Molecular docking of 3PO with MAO-B. IL-1β = Interleukin-1β, IL-6 = Interleukin-6, TNF-α = Tumor necrosis factor-α, NF-κB = Nuclear factor kappa B.

Article Snippet: The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

Techniques:

The molecular dynamics simulations profiles of the IL-1β-3PO complex. (A) RMSD values (Complex: IL-1β-3PO, Protein: IL-1β, Ligand: 3PO). (B) RMSF analysis. (C) Number of hydrogen bonds formed between IL-1β and 3PO during the simulation. (D) Rg analysis. (E) SASA analysis. (F) Gibbs free energy landscape (2D). (G) Gibbs free energy landscape (3D). (H) The lowest energy 3D conformation. (I) 2D patterns of bonds at the most stable condition of the complex. (J) Time evolution of the MM/GBSA binding free energy. (K) Decomposition of the MM/GBSA binding free energy. (L) Per-residue energy decomposition. RMSD = Root mean square deviation, RMSF = Root mean square fluctuation, Rg = Radius of gyration, SASA = Solvent accessible surface area.

Journal: Frontiers in Pharmacology

Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments

doi: 10.3389/fphar.2026.1790273

Figure Lengend Snippet: The molecular dynamics simulations profiles of the IL-1β-3PO complex. (A) RMSD values (Complex: IL-1β-3PO, Protein: IL-1β, Ligand: 3PO). (B) RMSF analysis. (C) Number of hydrogen bonds formed between IL-1β and 3PO during the simulation. (D) Rg analysis. (E) SASA analysis. (F) Gibbs free energy landscape (2D). (G) Gibbs free energy landscape (3D). (H) The lowest energy 3D conformation. (I) 2D patterns of bonds at the most stable condition of the complex. (J) Time evolution of the MM/GBSA binding free energy. (K) Decomposition of the MM/GBSA binding free energy. (L) Per-residue energy decomposition. RMSD = Root mean square deviation, RMSF = Root mean square fluctuation, Rg = Radius of gyration, SASA = Solvent accessible surface area.

Article Snippet: The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

Techniques: Binding Assay, Residue, Solvent

The molecular dynamics simulations profiles of the IL-6-3PO complex. (A) RMSD values (Complex: IL-6-3PO, Protein: IL-6, Ligand: 3PO). (B) RMSF analysis. (C) Number of hydrogen bonds formed between IL-6 and 3PO during the simulation. (D) Rg analysis. (E) SASA analysis. (F) Gibbs free energy landscape (2D). (G) Gibbs free energy landscape (3D). (H) The lowest energy 3D conformation. (I) 2D patterns of bonds at the most stable condition of the complex. (J) Time evolution of the MM/GBSA binding free energy. (K) Decomposition of the MM/GBSA binding free energy. (L) Per-residue energy decomposition.

Journal: Frontiers in Pharmacology

Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments

doi: 10.3389/fphar.2026.1790273

Figure Lengend Snippet: The molecular dynamics simulations profiles of the IL-6-3PO complex. (A) RMSD values (Complex: IL-6-3PO, Protein: IL-6, Ligand: 3PO). (B) RMSF analysis. (C) Number of hydrogen bonds formed between IL-6 and 3PO during the simulation. (D) Rg analysis. (E) SASA analysis. (F) Gibbs free energy landscape (2D). (G) Gibbs free energy landscape (3D). (H) The lowest energy 3D conformation. (I) 2D patterns of bonds at the most stable condition of the complex. (J) Time evolution of the MM/GBSA binding free energy. (K) Decomposition of the MM/GBSA binding free energy. (L) Per-residue energy decomposition.

Article Snippet: The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

Techniques: Binding Assay, Residue

The molecular dynamics simulations profiles of the TNF-α-3PO complex. (A) RMSD values (Complex: TNF-α-3PO, Protein: TNF-α, Ligand: 3PO). (B) RMSF analysis. (C) Number of hydrogen bonds formed between TNF-α and 3PO during the simulation. (D) Rg analysis. (E) SASA analysis. (F) Gibbs free energy landscape (2D). (G) Gibbs free energy landscape (3D). (H) The lowest energy 3D conformation. (I) 2D patterns of bonds at the most stable condition of the complex. (J) Time evolution of the MM/GBSA binding free energy. (K) Decomposition of the MM/GBSA binding free energy. (L) Per-residue energy decomposition.

Journal: Frontiers in Pharmacology

Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments

doi: 10.3389/fphar.2026.1790273

Figure Lengend Snippet: The molecular dynamics simulations profiles of the TNF-α-3PO complex. (A) RMSD values (Complex: TNF-α-3PO, Protein: TNF-α, Ligand: 3PO). (B) RMSF analysis. (C) Number of hydrogen bonds formed between TNF-α and 3PO during the simulation. (D) Rg analysis. (E) SASA analysis. (F) Gibbs free energy landscape (2D). (G) Gibbs free energy landscape (3D). (H) The lowest energy 3D conformation. (I) 2D patterns of bonds at the most stable condition of the complex. (J) Time evolution of the MM/GBSA binding free energy. (K) Decomposition of the MM/GBSA binding free energy. (L) Per-residue energy decomposition.

Article Snippet: The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

Techniques: Binding Assay, Residue

The molecular dynamics simulations profiles of NF-κB p65-3PO complex. (A) RMSD values (Complex: NF-κB p65-3PO, Protein: NF-κB p65 Ligand: 3PO). (B) RMSF analysis. (C) Number of hydrogen bonds formed between NF-κB p65 and 3PO during the simulation. (D) Rg analysis. (E) SASA analysis. (F) Gibbs free energy landscape (2D). (G) Gibbs free energy landscape (3D). (H) The lowest energy 3D conformation. (I) 2D patterns of bonds at the most stable condition of the complex. (J) Time evolution of the MM/GBSA binding free energy. (K) Decomposition of the MM/GBSA binding free energy. (L) Per-residue energy decomposition.

Journal: Frontiers in Pharmacology

Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments

doi: 10.3389/fphar.2026.1790273

Figure Lengend Snippet: The molecular dynamics simulations profiles of NF-κB p65-3PO complex. (A) RMSD values (Complex: NF-κB p65-3PO, Protein: NF-κB p65 Ligand: 3PO). (B) RMSF analysis. (C) Number of hydrogen bonds formed between NF-κB p65 and 3PO during the simulation. (D) Rg analysis. (E) SASA analysis. (F) Gibbs free energy landscape (2D). (G) Gibbs free energy landscape (3D). (H) The lowest energy 3D conformation. (I) 2D patterns of bonds at the most stable condition of the complex. (J) Time evolution of the MM/GBSA binding free energy. (K) Decomposition of the MM/GBSA binding free energy. (L) Per-residue energy decomposition.

Article Snippet: The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

Techniques: Binding Assay, Residue

PFKFB3 inhibitor 3PO attenuated airway inflammation in OVA-induced asthmatic mice. (A) A schematic diagram of the design of animal experiments. Mice were sensitized and challenged with OVA, followed by treatment with 3PO. (B) Survival rate of mice during the experiment (no mortality observed). (C) Body weight changes of mice throughout the protocol. (D) PFKFB3 expression in lung sections was detected by immunohistochemistry. Red arrows indicate PFKFB3-positive cells. Scale bar = 50 μm. (E) Quantitative analysis of PFKFB3-positive cells in lung tissues. (F–M) Levels of cytokines in BALF, including (F) IL-4, (G) IL-5, (H) IL-13, (I) IL-17A, (J) IL-1β, (K) TNF-α, (L) IL-6, and (M) IL-10. Data are presented as the mean ± SD (n = 5 per group). #P < 0.05, ##P < 0.01, ###P < 0.001, ####P < 0.0001 vs. the control group. *p < 0.05, **p < 0.01, ***p < 0.001 vs. the OVA group. BALF = Bronchoalveolar lavage fluid. IL-4 = Interleukin-4, IL-5 = Interleukin-5, IL-13 = Interleukin-13, IL-17A = Interleukin-17A, IL-10 = Interleukin-10.

Journal: Frontiers in Pharmacology

Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments

doi: 10.3389/fphar.2026.1790273

Figure Lengend Snippet: PFKFB3 inhibitor 3PO attenuated airway inflammation in OVA-induced asthmatic mice. (A) A schematic diagram of the design of animal experiments. Mice were sensitized and challenged with OVA, followed by treatment with 3PO. (B) Survival rate of mice during the experiment (no mortality observed). (C) Body weight changes of mice throughout the protocol. (D) PFKFB3 expression in lung sections was detected by immunohistochemistry. Red arrows indicate PFKFB3-positive cells. Scale bar = 50 μm. (E) Quantitative analysis of PFKFB3-positive cells in lung tissues. (F–M) Levels of cytokines in BALF, including (F) IL-4, (G) IL-5, (H) IL-13, (I) IL-17A, (J) IL-1β, (K) TNF-α, (L) IL-6, and (M) IL-10. Data are presented as the mean ± SD (n = 5 per group). #P < 0.05, ##P < 0.01, ###P < 0.001, ####P < 0.0001 vs. the control group. *p < 0.05, **p < 0.01, ***p < 0.001 vs. the OVA group. BALF = Bronchoalveolar lavage fluid. IL-4 = Interleukin-4, IL-5 = Interleukin-5, IL-13 = Interleukin-13, IL-17A = Interleukin-17A, IL-10 = Interleukin-10.

Article Snippet: The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

Techniques: Expressing, Immunohistochemistry, Control

PFKFB3 inhibitor 3PO attenuated airway inflammation in OVA-induced asthmatic mice. (A) Lactate levels, (B) IgE levels, and (C) CCL11 levels in BALF. (D) Total cell counts in BALF. (E) Representative images of H&E staining of lung tissue sections. Black arrows indicate eosinophils. Magnification: ×200 (upper panel) and 400× (lower panel). Scale bar = 50 μm. (F) Quantitative analysis of PAS-positive area in lung tissues. (G) Airway mucus secretion and goblet cell hyperplasia were detected using PAS staining. Scale bar = 50 μm. (H) Quantitative inflammatory cell infiltration scores. (I) Representative immunofluorescence staining for CCR3 (green) in bronchial regions; nuclei were stained with DAPI (blue). Magnification: ×200 (left panel) and 400× (right panel). Scale bar = 50 μm. Data are presented as the mean ± SD (n = 5 per group). ###P < 0.001, ####P < 0.0001 vs. the control group. **p < 0.01, ****p < 0.0001 vs. the OVA group. IgE = Immunoglobulin E, CCR3 = Chemokine (C-C motif) receptor 3, H&E = Hematoxylin and eosin, PAS = Periodic acid-Schiff, CCL11 = Chemokine (C-C motif) ligand 11.

Journal: Frontiers in Pharmacology

Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments

doi: 10.3389/fphar.2026.1790273

Figure Lengend Snippet: PFKFB3 inhibitor 3PO attenuated airway inflammation in OVA-induced asthmatic mice. (A) Lactate levels, (B) IgE levels, and (C) CCL11 levels in BALF. (D) Total cell counts in BALF. (E) Representative images of H&E staining of lung tissue sections. Black arrows indicate eosinophils. Magnification: ×200 (upper panel) and 400× (lower panel). Scale bar = 50 μm. (F) Quantitative analysis of PAS-positive area in lung tissues. (G) Airway mucus secretion and goblet cell hyperplasia were detected using PAS staining. Scale bar = 50 μm. (H) Quantitative inflammatory cell infiltration scores. (I) Representative immunofluorescence staining for CCR3 (green) in bronchial regions; nuclei were stained with DAPI (blue). Magnification: ×200 (left panel) and 400× (right panel). Scale bar = 50 μm. Data are presented as the mean ± SD (n = 5 per group). ###P < 0.001, ####P < 0.0001 vs. the control group. **p < 0.01, ****p < 0.0001 vs. the OVA group. IgE = Immunoglobulin E, CCR3 = Chemokine (C-C motif) receptor 3, H&E = Hematoxylin and eosin, PAS = Periodic acid-Schiff, CCL11 = Chemokine (C-C motif) ligand 11.

Article Snippet: The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

Techniques: Staining, Immunofluorescence, Control

PFKFB3 inhibitor 3PO inhibited the NF-κB signaling pathway activation in the OVA-induced asthma mouse models. (A) Western blot analysis of p-NF-κB P65, NF-κB P65, IKB, and β-actin protein expression. (B–D) Quantitative analysis of (B) p-NF-κB P65, (C) total NF-κB P65, and (D) IKB protein expression, normalized to β-actin. (E) Schematic diagram illustrating the effect of 3PO on OVA-induced airway inflammation in asthma. Data are presented as the mean ± SD. #P < 0.05, ##P < 0.01 vs. the control group. *p < 0.05 vs. the OVA group. ns = no significance. IKB = Inhibitor of nuclear factor kappa B.

Journal: Frontiers in Pharmacology

Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments

doi: 10.3389/fphar.2026.1790273

Figure Lengend Snippet: PFKFB3 inhibitor 3PO inhibited the NF-κB signaling pathway activation in the OVA-induced asthma mouse models. (A) Western blot analysis of p-NF-κB P65, NF-κB P65, IKB, and β-actin protein expression. (B–D) Quantitative analysis of (B) p-NF-κB P65, (C) total NF-κB P65, and (D) IKB protein expression, normalized to β-actin. (E) Schematic diagram illustrating the effect of 3PO on OVA-induced airway inflammation in asthma. Data are presented as the mean ± SD. #P < 0.05, ##P < 0.01 vs. the control group. *p < 0.05 vs. the OVA group. ns = no significance. IKB = Inhibitor of nuclear factor kappa B.

Article Snippet: The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

Techniques: Activation Assay, Western Blot, Expressing, Control

Journal: Journal of Ginseng Research

Article Title: Ginsenoside Re regulates PFKFB3-mediated glycolysis to inhibit endothelial cell migration to ameliorate atherosclerosis

doi: 10.1016/j.jgr.2025.11.012

Figure Lengend Snippet: Re inhibits glycolysis in mice. (A) Representative image of PFKFB3 expression in mouse aortic root detected by immunohistochemistry (IHC), n = 3, bar = 100 μm. (B) PFKFB3, HIF-1α, and HK2 mRNA levels in the aorta, n = 3. (C) Western blotting assay and quantitative data of HIF-1α, HK2, and PFKFB3 in aorta, n = 3. ### p < 0.001, ## p < 0.01, # p < 0.05, vs. control group, ∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05 vs. AS group.

Article Snippet: For immunohistochemical (IHC) staining, the primary antibody used was PFKFB3 (Cat. D7H4Q, Cell Signaling Technology Co., Ltd.), and the secondary antibody was Goat Anti-Rabbit IgG(H + C), HRP (Cat. 80800619, Biotech Co., Ltd).

Techniques: Expressing, Immunohistochemistry, Western Blot, Control

Journal: Journal of Ginseng Research

Article Title: Ginsenoside Re regulates PFKFB3-mediated glycolysis to inhibit endothelial cell migration to ameliorate atherosclerosis

doi: 10.1016/j.jgr.2025.11.012

Figure Lengend Snippet: Re inhibits ox-LDL-induced glycolysis of HUVECs. (A) Glucose uptake by HUVECs, n = 3. (B) Lactate efflux by HUVECs, n = 3. (C) mRNA expression of PFKFB3, HIF-1α, and HK2 in HUVECs, n = 3. (D) Structural formula of ginsenoside Re. (E–G) Predicted binding sites of Re to PFKFB3, HIF-1α, and HK2 by molecular docking. ### p < 0.001, ## p < 0.01, # p < 0.05, vs. control group; ∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05, vs. ox-LDL group.

Techniques: Expressing, Binding Assay, Control

Journal: Journal of Ginseng Research

Article Title: Ginsenoside Re regulates PFKFB3-mediated glycolysis to inhibit endothelial cell migration to ameliorate atherosclerosis

doi: 10.1016/j.jgr.2025.11.012

Figure Lengend Snippet: Re inhibits endothelial cell migration via the PFKFB3-HIF-1α/VEGFA-VEGFR2 signaling pathways. (A) Western blot assay and quantitative analysis of PFKFB3 in HUVECs, n = 3. (B) Cell viability of PFKFB3 overexpressing ECs measured by CCK-8 assay, n = 6. (C) Western blot assay and quantitative analysis of PFKFB3 in HUVECs, n = 3. (D–E) Representative images of HUVEC induced by ox-LDL for 0 h and 12 h in wound healing experiments (bar = 50 μm) and quantification of EC migration, n = 3. (F, G) Western blot assay and quantitative data of VE-cadherin, HIF-1α, VEGFA, and VEGFR2 in HUVECs, n = 3. ### p < 0.001, ## p < 0.01, # p < 0.05, vs. control group; ∗∗∗ p < 0.001, ∗∗ p < 0.01, ∗ p < 0.05, vs. ox-LDL group.

Techniques: Migration, Protein-Protein interactions, Western Blot, CCK-8 Assay, Control

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