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pfkfb3 inhibitor 3po  (MedChemExpress)


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    Structured Review

    MedChemExpress pfkfb3 inhibitor 3po
    Network pharmacology analysis of the <t>PFKFB3</t> inhibitor 3PO’s potential anti-asthma targets. (A) The chemical structure of <t>3PO.</t> (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.
    Pfkfb3 Inhibitor 3po, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 38 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pfkfb3+inhibitor+3po/3PO/pmc13083170-63-1-5
    Average 95 stars, based on 38 article reviews
    pfkfb3 inhibitor 3po - by Bioz Stars, 2026-10
    95/100 stars

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    1) Product Images from "Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments"

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

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2026.1790273

    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.
    Figure Legend 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.

    Techniques Used: 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.
    Figure Legend 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.

    Techniques Used:

    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.
    Figure Legend 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.

    Techniques Used: 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.
    Figure Legend 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.

    Techniques Used: 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.
    Figure Legend 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.

    Techniques Used: 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.
    Figure Legend 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.

    Techniques Used: 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.
    Figure Legend 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.

    Techniques Used: 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.
    Figure Legend 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.

    Techniques Used: 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.
    Figure Legend 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.

    Techniques Used: Activation Assay, Western Blot, Expressing, Control

    Related Articles

    Construct:

    Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments
    Article Snippet: The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).. The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

    Binding Assay:

    Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments
    Article Snippet: The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).. The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

    Residue:

    Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments
    Article Snippet: The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).. The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

    Solvent:

    Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments
    Article Snippet: The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).. The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

    Expressing:

    Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments
    Article Snippet: The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).. The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

    Immunohistochemistry:

    Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments
    Article Snippet: The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).. The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

    Control:

    Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments
    Article Snippet: The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).. The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

    Staining:

    Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments
    Article Snippet: The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).. The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

    Immunofluorescence:

    Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments
    Article Snippet: The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).. The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

    Activation Assay:

    Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments
    Article Snippet: The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).. The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.

    Western Blot:

    Article Title: Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, and in vivo experiments
    Article Snippet: The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).The primary antibodies were as follows: anti-chemokine (C-C motif) receptor 3 (CCR3) (22351-1-AP, Proteintech), anti-p-NF-κB p65 (TP56372, Abmart), anti-NF-κB p65 ( T55034 , Abmart), and anti-IKB-α ( T55026 , Abmart).. The PFKFB3 inhibitor 3PO (HY-19824, MedChemExpress) was used in the experiments.



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    Fig. 4. PI3K/Akt mediated SFI-related inhibition of glycolysis in HUVEC. KEGG analysis of DEGs between the LPS and SFI + LPS groups (A). HUVEC were pre- incubated with SFI (10 μl/ml) for 1h before LPS stimulation (1 μg/ml) for another 4 h. The protein levels of p-Akt were determined by Western blot (B). HUVEC were pre-incubated with Akt inhibitor MK-2206 (2 μM) for 1 h before stimulated with LPS (1 μg/ml) for another 4 h. The protein levels of VCAM1, Ang2, <t>PFKFB3,</t> and p- Akt were determined by immunoblot assay (C).
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    Fig. 4. PI3K/Akt mediated SFI-related inhibition of glycolysis in HUVEC. KEGG analysis of DEGs between the LPS and SFI + LPS groups (A). HUVEC were pre- incubated with SFI (10 μl/ml) for 1h before LPS stimulation (1 μg/ml) for another 4 h. The protein levels of p-Akt were determined by Western blot (B). HUVEC were pre-incubated with Akt inhibitor MK-2206 (2 μM) for 1 h before stimulated with LPS (1 μg/ml) for another 4 h. The protein levels of VCAM1, Ang2, <t>PFKFB3,</t> and p- Akt were determined by immunoblot assay (C).
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    Fig. 4. PI3K/Akt mediated SFI-related inhibition of glycolysis in HUVEC. KEGG analysis of DEGs between the LPS and SFI + LPS groups (A). HUVEC were pre- incubated with SFI (10 μl/ml) for 1h before LPS stimulation (1 μg/ml) for another 4 h. The protein levels of p-Akt were determined by Western blot (B). HUVEC were pre-incubated with Akt inhibitor MK-2206 (2 μM) for 1 h before stimulated with LPS (1 μg/ml) for another 4 h. The protein levels of VCAM1, Ang2, <t>PFKFB3,</t> and p- Akt were determined by immunoblot assay (C).
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    Fig. 4. PI3K/Akt mediated SFI-related inhibition of glycolysis in HUVEC. KEGG analysis of DEGs between the LPS and SFI + LPS groups (A). HUVEC were pre- incubated with SFI (10 μl/ml) for 1h before LPS stimulation (1 μg/ml) for another 4 h. The protein levels of p-Akt were determined by Western blot (B). HUVEC were pre-incubated with Akt inhibitor MK-2206 (2 μM) for 1 h before stimulated with LPS (1 μg/ml) for another 4 h. The protein levels of VCAM1, Ang2, <t>PFKFB3,</t> and p- Akt were determined by immunoblot assay (C).
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    Fig. 4. Chemotactic migration of HUVEC in response to treatment with EE and E4 (both 10−7 M) in the presence or absence of the <t>PFKFB3</t> inhibitor 3PO (40 μM). Boyden functional assays were run for 6 h incubation at 37◦C. Negative control: 1% FBS; positive control: 15% FBS. Cell migration was measured as optical density value of migrated cells and expressed relative to negative con trol (1% FBS). Data are expressed as mean ± SEM of n = 5 independent ex periments. t-test; *p < 0.05, **p < 0.01 vs 1% FBS, #p < 0.05 vs E4, §p < 0.05 vs EE.
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    Fig. 4. Chemotactic migration of HUVEC in response to treatment with EE and E4 (both 10−7 M) in the presence or absence of the <t>PFKFB3</t> inhibitor 3PO (40 μM). Boyden functional assays were run for 6 h incubation at 37◦C. Negative control: 1% FBS; positive control: 15% FBS. Cell migration was measured as optical density value of migrated cells and expressed relative to negative con trol (1% FBS). Data are expressed as mean ± SEM of n = 5 independent ex periments. t-test; *p < 0.05, **p < 0.01 vs 1% FBS, #p < 0.05 vs E4, §p < 0.05 vs EE.
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    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

    Fig. 4. PI3K/Akt mediated SFI-related inhibition of glycolysis in HUVEC. KEGG analysis of DEGs between the LPS and SFI + LPS groups (A). HUVEC were pre- incubated with SFI (10 μl/ml) for 1h before LPS stimulation (1 μg/ml) for another 4 h. The protein levels of p-Akt were determined by Western blot (B). HUVEC were pre-incubated with Akt inhibitor MK-2206 (2 μM) for 1 h before stimulated with LPS (1 μg/ml) for another 4 h. The protein levels of VCAM1, Ang2, PFKFB3, and p- Akt were determined by immunoblot assay (C).

    Journal: Journal of ethnopharmacology

    Article Title: Shenfu injection ameliorates endotoxemia-associated endothelial dysfunction and organ injury via inhibiting PI3K/Akt-mediated glycolysis.

    doi: 10.1016/j.jep.2024.118634

    Figure Lengend Snippet: Fig. 4. PI3K/Akt mediated SFI-related inhibition of glycolysis in HUVEC. KEGG analysis of DEGs between the LPS and SFI + LPS groups (A). HUVEC were pre- incubated with SFI (10 μl/ml) for 1h before LPS stimulation (1 μg/ml) for another 4 h. The protein levels of p-Akt were determined by Western blot (B). HUVEC were pre-incubated with Akt inhibitor MK-2206 (2 μM) for 1 h before stimulated with LPS (1 μg/ml) for another 4 h. The protein levels of VCAM1, Ang2, PFKFB3, and p- Akt were determined by immunoblot assay (C).

    Article Snippet: For intervention groups, HUVEC were pre-incubated with PFKFB3 inhibitor 3PO (10 μM, S7639, Selleck, Houston, TX, USA) or Akt inhibitor MK-2206 (2 μM, S1078, Selleck) for 1 h before stimulated with LPS (1 μg/ml) for another 4 h.

    Techniques: Inhibition, Incubation, Western Blot

    Fig. 4. Chemotactic migration of HUVEC in response to treatment with EE and E4 (both 10−7 M) in the presence or absence of the PFKFB3 inhibitor 3PO (40 μM). Boyden functional assays were run for 6 h incubation at 37◦C. Negative control: 1% FBS; positive control: 15% FBS. Cell migration was measured as optical density value of migrated cells and expressed relative to negative con trol (1% FBS). Data are expressed as mean ± SEM of n = 5 independent ex periments. t-test; *p < 0.05, **p < 0.01 vs 1% FBS, #p < 0.05 vs E4, §p < 0.05 vs EE.

    Journal: European journal of pharmacology

    Article Title: Regulation of human endothelial cell migration by oral contraceptive estrogen receptor ligands.

    doi: 10.1016/j.ejphar.2023.175591

    Figure Lengend Snippet: Fig. 4. Chemotactic migration of HUVEC in response to treatment with EE and E4 (both 10−7 M) in the presence or absence of the PFKFB3 inhibitor 3PO (40 μM). Boyden functional assays were run for 6 h incubation at 37◦C. Negative control: 1% FBS; positive control: 15% FBS. Cell migration was measured as optical density value of migrated cells and expressed relative to negative con trol (1% FBS). Data are expressed as mean ± SEM of n = 5 independent ex periments. t-test; *p < 0.05, **p < 0.01 vs 1% FBS, #p < 0.05 vs E4, §p < 0.05 vs EE.

    Article Snippet: The GPER antagonist (±) -(3aR*,4S*,9bS*)-4-(6-bromo-1,3-benzodioxol-5-yl)-3a,4,5,9b-tetrahydro-8-(1-methylethyl)-3H cyclopenta[c]quinoline (G36) and the PFKFB3 inhibitor 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO) were purchased from Tocris Bioscience (Bristol, United Kingdom).

    Techniques: Migration, Functional Assay, Incubation, Negative Control, Positive Control