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p38 mapk activator anisomycin  (MedChemExpress)


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    MedChemExpress p38 mapk activator anisomycin
    Identifying key signaling pathways and MF enrichment patterns associated with quercetin in synovitis. (A) GO enrichment analysis of potential of quercetin targets, showing the top 15 markedly enriched terms across three categories: BP, MF and CC; (B) KEGG pathway enrichment analysis of the predicted targets, displaying the top 15 markedly enriched signaling pathways. Notably, the IL-17, <t>MAPK,</t> TNF and PI3K-Akt pathways were among the most markedly enriched, suggesting that quercetin may exert anti-synovitis effects by modulating these inflammation-related pathways. GO, Gene Ontology; BP, Biological Process; MF, Molecular Function; CC, Cellular Component; KEGG, Kyoto Encyclopedia of Genes and Genomes.
    P38 Mapk Activator Anisomycin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 172 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 mapk activator anisomycin/product/MedChemExpress
    Average 96 stars, based on 172 article reviews
    p38 mapk activator anisomycin - by Bioz Stars, 2026-03
    96/100 stars

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    1) Product Images from "Targeting p38 MAPK signaling pathway: Quercetin as a novel therapy for TMJ synovitis"

    Article Title: Targeting p38 MAPK signaling pathway: Quercetin as a novel therapy for TMJ synovitis

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm.2025.5692

    Identifying key signaling pathways and MF enrichment patterns associated with quercetin in synovitis. (A) GO enrichment analysis of potential of quercetin targets, showing the top 15 markedly enriched terms across three categories: BP, MF and CC; (B) KEGG pathway enrichment analysis of the predicted targets, displaying the top 15 markedly enriched signaling pathways. Notably, the IL-17, MAPK, TNF and PI3K-Akt pathways were among the most markedly enriched, suggesting that quercetin may exert anti-synovitis effects by modulating these inflammation-related pathways. GO, Gene Ontology; BP, Biological Process; MF, Molecular Function; CC, Cellular Component; KEGG, Kyoto Encyclopedia of Genes and Genomes.
    Figure Legend Snippet: Identifying key signaling pathways and MF enrichment patterns associated with quercetin in synovitis. (A) GO enrichment analysis of potential of quercetin targets, showing the top 15 markedly enriched terms across three categories: BP, MF and CC; (B) KEGG pathway enrichment analysis of the predicted targets, displaying the top 15 markedly enriched signaling pathways. Notably, the IL-17, MAPK, TNF and PI3K-Akt pathways were among the most markedly enriched, suggesting that quercetin may exert anti-synovitis effects by modulating these inflammation-related pathways. GO, Gene Ontology; BP, Biological Process; MF, Molecular Function; CC, Cellular Component; KEGG, Kyoto Encyclopedia of Genes and Genomes.

    Techniques Used: Protein-Protein interactions

    Molecular docking validation of quercetin binding to key targets in the MAPK and IL-17 signaling pathways. Binding modes of quercetin with (A) MMP3, (B) MMP9, (C) MMP13, (D) MAPK1, (E) MAPK8 and (F) MAPK14. Each panel illustrates the complex's three-dimensional structure, the protein's electrostatic surface and the two-dimensional interaction map of the protein-ligand complex.
    Figure Legend Snippet: Molecular docking validation of quercetin binding to key targets in the MAPK and IL-17 signaling pathways. Binding modes of quercetin with (A) MMP3, (B) MMP9, (C) MMP13, (D) MAPK1, (E) MAPK8 and (F) MAPK14. Each panel illustrates the complex's three-dimensional structure, the protein's electrostatic surface and the two-dimensional interaction map of the protein-ligand complex.

    Techniques Used: Biomarker Discovery, Binding Assay, Protein-Protein interactions

    MD simulations evaluate the binding stability of quercetin with key target proteins. (A and B) The RMSD changes of each complex within 100 ns were evaluated to assess their overall structural stability; (C and D) RMSF analysis showing flexibility variations of individual protein residues; (E and F) Time-dependent changes in the number of hydrogen bonds, reflecting the physical stability of ligand binding; (G and H) Rg analysis assessing the compactness of protein structures. The results demonstrate that quercetin forms stable complexes with MMP and MAPK family targets. MD, Molecular Dynamics; RMSD, root-mean-square deviation; RMSF, root-mean-square fluctuation; Rg, radius of gyration; MMP, matrix metalloproteinase.
    Figure Legend Snippet: MD simulations evaluate the binding stability of quercetin with key target proteins. (A and B) The RMSD changes of each complex within 100 ns were evaluated to assess their overall structural stability; (C and D) RMSF analysis showing flexibility variations of individual protein residues; (E and F) Time-dependent changes in the number of hydrogen bonds, reflecting the physical stability of ligand binding; (G and H) Rg analysis assessing the compactness of protein structures. The results demonstrate that quercetin forms stable complexes with MMP and MAPK family targets. MD, Molecular Dynamics; RMSD, root-mean-square deviation; RMSF, root-mean-square fluctuation; Rg, radius of gyration; MMP, matrix metalloproteinase.

    Techniques Used: Binding Assay, Ligand Binding Assay

    Multi-level validation of quercetin-mediated regulation of inflammatory cytokines and MMPs via inhibition of the p38 MAPK signaling pathway. (A) ELISA analysis showing the effects of different concentrations of quercetin on IL-1β-induced secretion of MMP3, MMP9 and MMP13 in SW982 cells; (B) Western blot analysis of TNF-α, IL-1β and IL-6 protein expression levels, with β-tubulin as the internal control; (C and D) Western blot analysis of phosphorylation levels of key MAPK signaling molecules: p38, ERK1/2 and JNK; (E) Quantitative analysis of phosphorylated proteins, showing that quercetin markedly inhibited the expression of p-p38 and p-JNK, with no significant effect on p-ERK1/2. All experiments were independently repeated three times (n=3) and data are presented as mean ± SD. Statistical comparisons were performed using one-way ANOVA. Significance levels compared with the model group or 0 μ M group are indicated as: * P<0.05, ** P<0.01, *** P<0.001; ns: insignificant. MMPs, matrix metalloproteinases; ELISA, enzyme-linked immunosorbent assay; p-, phosphorylated.
    Figure Legend Snippet: Multi-level validation of quercetin-mediated regulation of inflammatory cytokines and MMPs via inhibition of the p38 MAPK signaling pathway. (A) ELISA analysis showing the effects of different concentrations of quercetin on IL-1β-induced secretion of MMP3, MMP9 and MMP13 in SW982 cells; (B) Western blot analysis of TNF-α, IL-1β and IL-6 protein expression levels, with β-tubulin as the internal control; (C and D) Western blot analysis of phosphorylation levels of key MAPK signaling molecules: p38, ERK1/2 and JNK; (E) Quantitative analysis of phosphorylated proteins, showing that quercetin markedly inhibited the expression of p-p38 and p-JNK, with no significant effect on p-ERK1/2. All experiments were independently repeated three times (n=3) and data are presented as mean ± SD. Statistical comparisons were performed using one-way ANOVA. Significance levels compared with the model group or 0 μ M group are indicated as: * P<0.05, ** P<0.01, *** P<0.001; ns: insignificant. MMPs, matrix metalloproteinases; ELISA, enzyme-linked immunosorbent assay; p-, phosphorylated.

    Techniques Used: Biomarker Discovery, Inhibition, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Control, Phospho-proteomics

    Multi-level analysis validates quercetin's therapeutic effects on synovitis and its regulatory role in inflammation-related signaling pathways. (A) H&E staining assessing changes in synovial structure and inflammatory cell infiltration. (B) Safranin O-Fast Green staining showing alterations in proteoglycan distribution in condylar cartilage. (C) Dual immunofluorescence staining analyzing the co-localization of p-p38 MAPK (green) with IL-6 (red) and MMP13 (red) in synovial tissue. (D) qPCR analysis of key gene expression levels, including MAPK14, MAPKAPK2, DUSP1, IL-6, TNF-α and MMP13, in SW982 cells and synovial tissues. All histological experiments were conducted with five animals per group (n=5) and molecular experiments were independently repeated three times (n=3). Data are presented as mean ± SD. Statistical comparisons were performed using one-way ANOVA. Significance levels: * P<0.05, ** P<0.01, *** P<0.001, **** P<0.0001; ns, insignificant. H&E, hematoxylin and eosin; MMP, matrix metalloproteinase; qPCR, quantitative PCR.
    Figure Legend Snippet: Multi-level analysis validates quercetin's therapeutic effects on synovitis and its regulatory role in inflammation-related signaling pathways. (A) H&E staining assessing changes in synovial structure and inflammatory cell infiltration. (B) Safranin O-Fast Green staining showing alterations in proteoglycan distribution in condylar cartilage. (C) Dual immunofluorescence staining analyzing the co-localization of p-p38 MAPK (green) with IL-6 (red) and MMP13 (red) in synovial tissue. (D) qPCR analysis of key gene expression levels, including MAPK14, MAPKAPK2, DUSP1, IL-6, TNF-α and MMP13, in SW982 cells and synovial tissues. All histological experiments were conducted with five animals per group (n=5) and molecular experiments were independently repeated three times (n=3). Data are presented as mean ± SD. Statistical comparisons were performed using one-way ANOVA. Significance levels: * P<0.05, ** P<0.01, *** P<0.001, **** P<0.0001; ns, insignificant. H&E, hematoxylin and eosin; MMP, matrix metalloproteinase; qPCR, quantitative PCR.

    Techniques Used: Protein-Protein interactions, Staining, Immunofluorescence, Gene Expression, Real-time Polymerase Chain Reaction

    Quercetin alleviates inflammatory cytokine expression and mitigates bone destruction by modulating the p38 MAPK signaling pathway. (A) InstantOne ELISA analysis of p-p38 MAPK, p-JNK and p-ERK levels in synovial tissue. (B) IHC staining showing expression changes of MMP13, IL-6 and p-p38 MAPK in synovial tissue. (C) Evaluation of subchondral bone destruction using Micro-CT sagittal slices, (D and E) 3D reconstructions and (F) cylindrical ROI of rat condylar bone. (G) Quantitative analysis of BV/TV, Tb.N and Tb.Sp. Scale bar, 500 μ m. Comparisons were made against the CFA group. Each group included five rats (n=5) and data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA; * P<0.05, ** P<0.01, *** P<0.001. ELISA, enzyme-linked immunosorbent assay; p-, phosphorylated; IHC, immunohistochemistry; MMP, matrix metalloproteinase; Micro-CT, micro-computed tomography; ROI, region of interest; BV/TV, bone volume/tissue volume; Tb.N, trabecular number; Tb.Sp, trabecular separation; CFA, Complete Freund's Adjuvant.
    Figure Legend Snippet: Quercetin alleviates inflammatory cytokine expression and mitigates bone destruction by modulating the p38 MAPK signaling pathway. (A) InstantOne ELISA analysis of p-p38 MAPK, p-JNK and p-ERK levels in synovial tissue. (B) IHC staining showing expression changes of MMP13, IL-6 and p-p38 MAPK in synovial tissue. (C) Evaluation of subchondral bone destruction using Micro-CT sagittal slices, (D and E) 3D reconstructions and (F) cylindrical ROI of rat condylar bone. (G) Quantitative analysis of BV/TV, Tb.N and Tb.Sp. Scale bar, 500 μ m. Comparisons were made against the CFA group. Each group included five rats (n=5) and data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA; * P<0.05, ** P<0.01, *** P<0.001. ELISA, enzyme-linked immunosorbent assay; p-, phosphorylated; IHC, immunohistochemistry; MMP, matrix metalloproteinase; Micro-CT, micro-computed tomography; ROI, region of interest; BV/TV, bone volume/tissue volume; Tb.N, trabecular number; Tb.Sp, trabecular separation; CFA, Complete Freund's Adjuvant.

    Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay, Immunohistochemistry, Micro-CT, Adjuvant

    Agonist/inhibitor experiments confirm that the anti-inflammatory mechanism of quercetin depends on the p38 MAPK signaling pathway. (A) Western blot analysis of p-p38 MAPK protein expression. (B) ELISA detection of IL-6 and TNF-α secretion levels (pg/ml). (C) CCK-8 assay for evaluating cell proliferation activity (OD450). (D) Annexin V/PI flow cytometry analysis of apoptosis rate (%). Experimental groups included: Control, IL-1β, IL-1β + quercetin, IL-1β + quercetin + SB203580 and IL-1β + quercetin + anisomycin. All experiments were independently repeated three times (n=3) and data are expressed as mean ± SD. Statistical comparisons were performed using one-way ANOVA; * P<0.05, ** P<0.01, *** P<0.001 **** P<0.0001; ns: insignificant. p-, phosphorylated; ELISA, enzyme-linked immunosorbent assay; CCK-8, Cell Counting Kit-8; OD, optical density.
    Figure Legend Snippet: Agonist/inhibitor experiments confirm that the anti-inflammatory mechanism of quercetin depends on the p38 MAPK signaling pathway. (A) Western blot analysis of p-p38 MAPK protein expression. (B) ELISA detection of IL-6 and TNF-α secretion levels (pg/ml). (C) CCK-8 assay for evaluating cell proliferation activity (OD450). (D) Annexin V/PI flow cytometry analysis of apoptosis rate (%). Experimental groups included: Control, IL-1β, IL-1β + quercetin, IL-1β + quercetin + SB203580 and IL-1β + quercetin + anisomycin. All experiments were independently repeated three times (n=3) and data are expressed as mean ± SD. Statistical comparisons were performed using one-way ANOVA; * P<0.05, ** P<0.01, *** P<0.001 **** P<0.0001; ns: insignificant. p-, phosphorylated; ELISA, enzyme-linked immunosorbent assay; CCK-8, Cell Counting Kit-8; OD, optical density.

    Techniques Used: Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Activity Assay, Flow Cytometry, Control, Cell Counting



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    Image Search Results


    Identifying key signaling pathways and MF enrichment patterns associated with quercetin in synovitis. (A) GO enrichment analysis of potential of quercetin targets, showing the top 15 markedly enriched terms across three categories: BP, MF and CC; (B) KEGG pathway enrichment analysis of the predicted targets, displaying the top 15 markedly enriched signaling pathways. Notably, the IL-17, MAPK, TNF and PI3K-Akt pathways were among the most markedly enriched, suggesting that quercetin may exert anti-synovitis effects by modulating these inflammation-related pathways. GO, Gene Ontology; BP, Biological Process; MF, Molecular Function; CC, Cellular Component; KEGG, Kyoto Encyclopedia of Genes and Genomes.

    Journal: International Journal of Molecular Medicine

    Article Title: Targeting p38 MAPK signaling pathway: Quercetin as a novel therapy for TMJ synovitis

    doi: 10.3892/ijmm.2025.5692

    Figure Lengend Snippet: Identifying key signaling pathways and MF enrichment patterns associated with quercetin in synovitis. (A) GO enrichment analysis of potential of quercetin targets, showing the top 15 markedly enriched terms across three categories: BP, MF and CC; (B) KEGG pathway enrichment analysis of the predicted targets, displaying the top 15 markedly enriched signaling pathways. Notably, the IL-17, MAPK, TNF and PI3K-Akt pathways were among the most markedly enriched, suggesting that quercetin may exert anti-synovitis effects by modulating these inflammation-related pathways. GO, Gene Ontology; BP, Biological Process; MF, Molecular Function; CC, Cellular Component; KEGG, Kyoto Encyclopedia of Genes and Genomes.

    Article Snippet: After 24 h of IL-1β (10 ng/ml) stimulation, SW982 cells were pretreated for 30 min with either the p38 MAPK activator anisomycin (10 μ M; MedChemExpress; cat. no. HY-18982) or the inhibitor SB203580 (10 μ M, HY-10256, MedChemExpress), followed by co-treatment with 40 μ M quercetin for another 24 h ( , ).

    Techniques: Protein-Protein interactions

    Molecular docking validation of quercetin binding to key targets in the MAPK and IL-17 signaling pathways. Binding modes of quercetin with (A) MMP3, (B) MMP9, (C) MMP13, (D) MAPK1, (E) MAPK8 and (F) MAPK14. Each panel illustrates the complex's three-dimensional structure, the protein's electrostatic surface and the two-dimensional interaction map of the protein-ligand complex.

    Journal: International Journal of Molecular Medicine

    Article Title: Targeting p38 MAPK signaling pathway: Quercetin as a novel therapy for TMJ synovitis

    doi: 10.3892/ijmm.2025.5692

    Figure Lengend Snippet: Molecular docking validation of quercetin binding to key targets in the MAPK and IL-17 signaling pathways. Binding modes of quercetin with (A) MMP3, (B) MMP9, (C) MMP13, (D) MAPK1, (E) MAPK8 and (F) MAPK14. Each panel illustrates the complex's three-dimensional structure, the protein's electrostatic surface and the two-dimensional interaction map of the protein-ligand complex.

    Article Snippet: After 24 h of IL-1β (10 ng/ml) stimulation, SW982 cells were pretreated for 30 min with either the p38 MAPK activator anisomycin (10 μ M; MedChemExpress; cat. no. HY-18982) or the inhibitor SB203580 (10 μ M, HY-10256, MedChemExpress), followed by co-treatment with 40 μ M quercetin for another 24 h ( , ).

    Techniques: Biomarker Discovery, Binding Assay, Protein-Protein interactions

    MD simulations evaluate the binding stability of quercetin with key target proteins. (A and B) The RMSD changes of each complex within 100 ns were evaluated to assess their overall structural stability; (C and D) RMSF analysis showing flexibility variations of individual protein residues; (E and F) Time-dependent changes in the number of hydrogen bonds, reflecting the physical stability of ligand binding; (G and H) Rg analysis assessing the compactness of protein structures. The results demonstrate that quercetin forms stable complexes with MMP and MAPK family targets. MD, Molecular Dynamics; RMSD, root-mean-square deviation; RMSF, root-mean-square fluctuation; Rg, radius of gyration; MMP, matrix metalloproteinase.

    Journal: International Journal of Molecular Medicine

    Article Title: Targeting p38 MAPK signaling pathway: Quercetin as a novel therapy for TMJ synovitis

    doi: 10.3892/ijmm.2025.5692

    Figure Lengend Snippet: MD simulations evaluate the binding stability of quercetin with key target proteins. (A and B) The RMSD changes of each complex within 100 ns were evaluated to assess their overall structural stability; (C and D) RMSF analysis showing flexibility variations of individual protein residues; (E and F) Time-dependent changes in the number of hydrogen bonds, reflecting the physical stability of ligand binding; (G and H) Rg analysis assessing the compactness of protein structures. The results demonstrate that quercetin forms stable complexes with MMP and MAPK family targets. MD, Molecular Dynamics; RMSD, root-mean-square deviation; RMSF, root-mean-square fluctuation; Rg, radius of gyration; MMP, matrix metalloproteinase.

    Article Snippet: After 24 h of IL-1β (10 ng/ml) stimulation, SW982 cells were pretreated for 30 min with either the p38 MAPK activator anisomycin (10 μ M; MedChemExpress; cat. no. HY-18982) or the inhibitor SB203580 (10 μ M, HY-10256, MedChemExpress), followed by co-treatment with 40 μ M quercetin for another 24 h ( , ).

    Techniques: Binding Assay, Ligand Binding Assay

    Multi-level validation of quercetin-mediated regulation of inflammatory cytokines and MMPs via inhibition of the p38 MAPK signaling pathway. (A) ELISA analysis showing the effects of different concentrations of quercetin on IL-1β-induced secretion of MMP3, MMP9 and MMP13 in SW982 cells; (B) Western blot analysis of TNF-α, IL-1β and IL-6 protein expression levels, with β-tubulin as the internal control; (C and D) Western blot analysis of phosphorylation levels of key MAPK signaling molecules: p38, ERK1/2 and JNK; (E) Quantitative analysis of phosphorylated proteins, showing that quercetin markedly inhibited the expression of p-p38 and p-JNK, with no significant effect on p-ERK1/2. All experiments were independently repeated three times (n=3) and data are presented as mean ± SD. Statistical comparisons were performed using one-way ANOVA. Significance levels compared with the model group or 0 μ M group are indicated as: * P<0.05, ** P<0.01, *** P<0.001; ns: insignificant. MMPs, matrix metalloproteinases; ELISA, enzyme-linked immunosorbent assay; p-, phosphorylated.

    Journal: International Journal of Molecular Medicine

    Article Title: Targeting p38 MAPK signaling pathway: Quercetin as a novel therapy for TMJ synovitis

    doi: 10.3892/ijmm.2025.5692

    Figure Lengend Snippet: Multi-level validation of quercetin-mediated regulation of inflammatory cytokines and MMPs via inhibition of the p38 MAPK signaling pathway. (A) ELISA analysis showing the effects of different concentrations of quercetin on IL-1β-induced secretion of MMP3, MMP9 and MMP13 in SW982 cells; (B) Western blot analysis of TNF-α, IL-1β and IL-6 protein expression levels, with β-tubulin as the internal control; (C and D) Western blot analysis of phosphorylation levels of key MAPK signaling molecules: p38, ERK1/2 and JNK; (E) Quantitative analysis of phosphorylated proteins, showing that quercetin markedly inhibited the expression of p-p38 and p-JNK, with no significant effect on p-ERK1/2. All experiments were independently repeated three times (n=3) and data are presented as mean ± SD. Statistical comparisons were performed using one-way ANOVA. Significance levels compared with the model group or 0 μ M group are indicated as: * P<0.05, ** P<0.01, *** P<0.001; ns: insignificant. MMPs, matrix metalloproteinases; ELISA, enzyme-linked immunosorbent assay; p-, phosphorylated.

    Article Snippet: After 24 h of IL-1β (10 ng/ml) stimulation, SW982 cells were pretreated for 30 min with either the p38 MAPK activator anisomycin (10 μ M; MedChemExpress; cat. no. HY-18982) or the inhibitor SB203580 (10 μ M, HY-10256, MedChemExpress), followed by co-treatment with 40 μ M quercetin for another 24 h ( , ).

    Techniques: Biomarker Discovery, Inhibition, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Control, Phospho-proteomics

    Multi-level analysis validates quercetin's therapeutic effects on synovitis and its regulatory role in inflammation-related signaling pathways. (A) H&E staining assessing changes in synovial structure and inflammatory cell infiltration. (B) Safranin O-Fast Green staining showing alterations in proteoglycan distribution in condylar cartilage. (C) Dual immunofluorescence staining analyzing the co-localization of p-p38 MAPK (green) with IL-6 (red) and MMP13 (red) in synovial tissue. (D) qPCR analysis of key gene expression levels, including MAPK14, MAPKAPK2, DUSP1, IL-6, TNF-α and MMP13, in SW982 cells and synovial tissues. All histological experiments were conducted with five animals per group (n=5) and molecular experiments were independently repeated three times (n=3). Data are presented as mean ± SD. Statistical comparisons were performed using one-way ANOVA. Significance levels: * P<0.05, ** P<0.01, *** P<0.001, **** P<0.0001; ns, insignificant. H&E, hematoxylin and eosin; MMP, matrix metalloproteinase; qPCR, quantitative PCR.

    Journal: International Journal of Molecular Medicine

    Article Title: Targeting p38 MAPK signaling pathway: Quercetin as a novel therapy for TMJ synovitis

    doi: 10.3892/ijmm.2025.5692

    Figure Lengend Snippet: Multi-level analysis validates quercetin's therapeutic effects on synovitis and its regulatory role in inflammation-related signaling pathways. (A) H&E staining assessing changes in synovial structure and inflammatory cell infiltration. (B) Safranin O-Fast Green staining showing alterations in proteoglycan distribution in condylar cartilage. (C) Dual immunofluorescence staining analyzing the co-localization of p-p38 MAPK (green) with IL-6 (red) and MMP13 (red) in synovial tissue. (D) qPCR analysis of key gene expression levels, including MAPK14, MAPKAPK2, DUSP1, IL-6, TNF-α and MMP13, in SW982 cells and synovial tissues. All histological experiments were conducted with five animals per group (n=5) and molecular experiments were independently repeated three times (n=3). Data are presented as mean ± SD. Statistical comparisons were performed using one-way ANOVA. Significance levels: * P<0.05, ** P<0.01, *** P<0.001, **** P<0.0001; ns, insignificant. H&E, hematoxylin and eosin; MMP, matrix metalloproteinase; qPCR, quantitative PCR.

    Article Snippet: After 24 h of IL-1β (10 ng/ml) stimulation, SW982 cells were pretreated for 30 min with either the p38 MAPK activator anisomycin (10 μ M; MedChemExpress; cat. no. HY-18982) or the inhibitor SB203580 (10 μ M, HY-10256, MedChemExpress), followed by co-treatment with 40 μ M quercetin for another 24 h ( , ).

    Techniques: Protein-Protein interactions, Staining, Immunofluorescence, Gene Expression, Real-time Polymerase Chain Reaction

    Quercetin alleviates inflammatory cytokine expression and mitigates bone destruction by modulating the p38 MAPK signaling pathway. (A) InstantOne ELISA analysis of p-p38 MAPK, p-JNK and p-ERK levels in synovial tissue. (B) IHC staining showing expression changes of MMP13, IL-6 and p-p38 MAPK in synovial tissue. (C) Evaluation of subchondral bone destruction using Micro-CT sagittal slices, (D and E) 3D reconstructions and (F) cylindrical ROI of rat condylar bone. (G) Quantitative analysis of BV/TV, Tb.N and Tb.Sp. Scale bar, 500 μ m. Comparisons were made against the CFA group. Each group included five rats (n=5) and data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA; * P<0.05, ** P<0.01, *** P<0.001. ELISA, enzyme-linked immunosorbent assay; p-, phosphorylated; IHC, immunohistochemistry; MMP, matrix metalloproteinase; Micro-CT, micro-computed tomography; ROI, region of interest; BV/TV, bone volume/tissue volume; Tb.N, trabecular number; Tb.Sp, trabecular separation; CFA, Complete Freund's Adjuvant.

    Journal: International Journal of Molecular Medicine

    Article Title: Targeting p38 MAPK signaling pathway: Quercetin as a novel therapy for TMJ synovitis

    doi: 10.3892/ijmm.2025.5692

    Figure Lengend Snippet: Quercetin alleviates inflammatory cytokine expression and mitigates bone destruction by modulating the p38 MAPK signaling pathway. (A) InstantOne ELISA analysis of p-p38 MAPK, p-JNK and p-ERK levels in synovial tissue. (B) IHC staining showing expression changes of MMP13, IL-6 and p-p38 MAPK in synovial tissue. (C) Evaluation of subchondral bone destruction using Micro-CT sagittal slices, (D and E) 3D reconstructions and (F) cylindrical ROI of rat condylar bone. (G) Quantitative analysis of BV/TV, Tb.N and Tb.Sp. Scale bar, 500 μ m. Comparisons were made against the CFA group. Each group included five rats (n=5) and data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA; * P<0.05, ** P<0.01, *** P<0.001. ELISA, enzyme-linked immunosorbent assay; p-, phosphorylated; IHC, immunohistochemistry; MMP, matrix metalloproteinase; Micro-CT, micro-computed tomography; ROI, region of interest; BV/TV, bone volume/tissue volume; Tb.N, trabecular number; Tb.Sp, trabecular separation; CFA, Complete Freund's Adjuvant.

    Article Snippet: After 24 h of IL-1β (10 ng/ml) stimulation, SW982 cells were pretreated for 30 min with either the p38 MAPK activator anisomycin (10 μ M; MedChemExpress; cat. no. HY-18982) or the inhibitor SB203580 (10 μ M, HY-10256, MedChemExpress), followed by co-treatment with 40 μ M quercetin for another 24 h ( , ).

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Immunohistochemistry, Micro-CT, Adjuvant

    Agonist/inhibitor experiments confirm that the anti-inflammatory mechanism of quercetin depends on the p38 MAPK signaling pathway. (A) Western blot analysis of p-p38 MAPK protein expression. (B) ELISA detection of IL-6 and TNF-α secretion levels (pg/ml). (C) CCK-8 assay for evaluating cell proliferation activity (OD450). (D) Annexin V/PI flow cytometry analysis of apoptosis rate (%). Experimental groups included: Control, IL-1β, IL-1β + quercetin, IL-1β + quercetin + SB203580 and IL-1β + quercetin + anisomycin. All experiments were independently repeated three times (n=3) and data are expressed as mean ± SD. Statistical comparisons were performed using one-way ANOVA; * P<0.05, ** P<0.01, *** P<0.001 **** P<0.0001; ns: insignificant. p-, phosphorylated; ELISA, enzyme-linked immunosorbent assay; CCK-8, Cell Counting Kit-8; OD, optical density.

    Journal: International Journal of Molecular Medicine

    Article Title: Targeting p38 MAPK signaling pathway: Quercetin as a novel therapy for TMJ synovitis

    doi: 10.3892/ijmm.2025.5692

    Figure Lengend Snippet: Agonist/inhibitor experiments confirm that the anti-inflammatory mechanism of quercetin depends on the p38 MAPK signaling pathway. (A) Western blot analysis of p-p38 MAPK protein expression. (B) ELISA detection of IL-6 and TNF-α secretion levels (pg/ml). (C) CCK-8 assay for evaluating cell proliferation activity (OD450). (D) Annexin V/PI flow cytometry analysis of apoptosis rate (%). Experimental groups included: Control, IL-1β, IL-1β + quercetin, IL-1β + quercetin + SB203580 and IL-1β + quercetin + anisomycin. All experiments were independently repeated three times (n=3) and data are expressed as mean ± SD. Statistical comparisons were performed using one-way ANOVA; * P<0.05, ** P<0.01, *** P<0.001 **** P<0.0001; ns: insignificant. p-, phosphorylated; ELISA, enzyme-linked immunosorbent assay; CCK-8, Cell Counting Kit-8; OD, optical density.

    Article Snippet: After 24 h of IL-1β (10 ng/ml) stimulation, SW982 cells were pretreated for 30 min with either the p38 MAPK activator anisomycin (10 μ M; MedChemExpress; cat. no. HY-18982) or the inhibitor SB203580 (10 μ M, HY-10256, MedChemExpress), followed by co-treatment with 40 μ M quercetin for another 24 h ( , ).

    Techniques: Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Activity Assay, Flow Cytometry, Control, Cell Counting

    Effects of vancomycin (Vanco) and lycopene (Lyco) administrations on (A) nuclear factor kappa B (NF‐κB), (B) tumour necrosis factor‐alpha (TNF‐ α ), (C) B‐cell lymphoma 3 (Bcl‐3) and (D) mitogen‐activated protein kinase p38 alpha (p38 α MAPK) levels in kidney tissues of rats. Values are given as mean ± SD CO Control versus others: * p < 0.05, ** p < 0.01, *** p < 0.001; Vanco versus others: # p < 0.05, ## p < 0.01, ### p < 0.001; Vanco + Lyco 5 versus Vanco + Lyco 10: & p < 0.05, && p < 0.01, &&& p < 0.001.

    Journal: Basic & Clinical Pharmacology & Toxicology

    Article Title: Antioxidant, Antiinflammatory and Antiapoptotic Effects of Lycopene in Rats With Vancomycin‐Induced Nephrotoxicity

    doi: 10.1111/bcpt.70084

    Figure Lengend Snippet: Effects of vancomycin (Vanco) and lycopene (Lyco) administrations on (A) nuclear factor kappa B (NF‐κB), (B) tumour necrosis factor‐alpha (TNF‐ α ), (C) B‐cell lymphoma 3 (Bcl‐3) and (D) mitogen‐activated protein kinase p38 alpha (p38 α MAPK) levels in kidney tissues of rats. Values are given as mean ± SD CO Control versus others: * p < 0.05, ** p < 0.01, *** p < 0.001; Vanco versus others: # p < 0.05, ## p < 0.01, ### p < 0.001; Vanco + Lyco 5 versus Vanco + Lyco 10: & p < 0.05, && p < 0.01, &&& p < 0.001.

    Article Snippet: Nuclear Factor kappa B (NF‐κB; product no: SEB824Ra), tumour necrosis factor‐alpha (TNF‐ α ; product no: SEA133Ra) and B‐cell lymphoma 3 (Bcl‐3; Product No: SEB734Ra) levels (Cloud‐Clone Corp. [CCC, TX, USA]) and mitogen‐activated protein kinase p38 alpha ([p38 α MAPK; Catalogue No: CK‐bio‐25 173], Shanghai Coon Koon Biotech Co Ltd. [Shanghai, China]) activity were decided with commercial ELISA kits consistent with the manufacturer's instructions.

    Techniques: Control