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ards nsc95397  (MedChemExpress)


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    Structured Review

    MedChemExpress ards nsc95397
    Proinflammatory cytokine genes were predominately upregulated in <t>ARDS</t> mice. (A) Experimental design: RNA-Seq analysis to identify differentially expressed genes (DGEs) in ARDS mice. (B) Volcano plot displaying RNA-Seq results. (C) Heatmap of top 20 upregulated genes and top 10 downregulated genes in ARDS lung tissues. (D) Biological processes of DGEs revealed by gene ontology (GO) analysis. (E and F) Verification of 12 DGEs by RT-qPCR analysis ( n = 3). (E) IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG. (F) S100A8, CtBP2, ICAM1, SPP1, FBN1, and SPSB1. ** P < 0.01; *** P < 0.001
    Ards Nsc95397, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ards nsc95397/product/MedChemExpress
    Average 93 stars, based on 10 article reviews
    ards nsc95397 - by Bioz Stars, 2026-03
    93/100 stars

    Images

    1) Product Images from "PNSC928, a plant-derived compound, specifically disrupts CtBP2-p300 interaction and reduces inflammation in mice with acute respiratory distress syndrome"

    Article Title: PNSC928, a plant-derived compound, specifically disrupts CtBP2-p300 interaction and reduces inflammation in mice with acute respiratory distress syndrome

    Journal: Biology Direct

    doi: 10.1186/s13062-024-00491-0

    Proinflammatory cytokine genes were predominately upregulated in ARDS mice. (A) Experimental design: RNA-Seq analysis to identify differentially expressed genes (DGEs) in ARDS mice. (B) Volcano plot displaying RNA-Seq results. (C) Heatmap of top 20 upregulated genes and top 10 downregulated genes in ARDS lung tissues. (D) Biological processes of DGEs revealed by gene ontology (GO) analysis. (E and F) Verification of 12 DGEs by RT-qPCR analysis ( n = 3). (E) IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG. (F) S100A8, CtBP2, ICAM1, SPP1, FBN1, and SPSB1. ** P < 0.01; *** P < 0.001
    Figure Legend Snippet: Proinflammatory cytokine genes were predominately upregulated in ARDS mice. (A) Experimental design: RNA-Seq analysis to identify differentially expressed genes (DGEs) in ARDS mice. (B) Volcano plot displaying RNA-Seq results. (C) Heatmap of top 20 upregulated genes and top 10 downregulated genes in ARDS lung tissues. (D) Biological processes of DGEs revealed by gene ontology (GO) analysis. (E and F) Verification of 12 DGEs by RT-qPCR analysis ( n = 3). (E) IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG. (F) S100A8, CtBP2, ICAM1, SPP1, FBN1, and SPSB1. ** P < 0.01; *** P < 0.001

    Techniques Used: RNA Sequencing Assay, Quantitative RT-PCR

    Inhibitors of CtBP2, p300, and NF-κB exhibited cytotoxicity in vivo. C57BL/6 mice were administrated with MTOB (400 and 800 mg/kg), NSC95397 (2 and 4 mg/kg), C646 (5 and 10 mg/kg), A-485 (40 and 80 mg/kg), TPCA1 (10 and 20 mg/kg), BOT64 (30 and 60 mg/kg) for a duration of 6 days ( n = 10 for each group). (A-F) Body weights were measured every two days. (G-K) Serum concentrations of different groups of mice. (G) IL-1β, (H) IL-6, (I) IL-15, (J) IL-18, and (K) TNF-α. * P < 0.05
    Figure Legend Snippet: Inhibitors of CtBP2, p300, and NF-κB exhibited cytotoxicity in vivo. C57BL/6 mice were administrated with MTOB (400 and 800 mg/kg), NSC95397 (2 and 4 mg/kg), C646 (5 and 10 mg/kg), A-485 (40 and 80 mg/kg), TPCA1 (10 and 20 mg/kg), BOT64 (30 and 60 mg/kg) for a duration of 6 days ( n = 10 for each group). (A-F) Body weights were measured every two days. (G-K) Serum concentrations of different groups of mice. (G) IL-1β, (H) IL-6, (I) IL-15, (J) IL-18, and (K) TNF-α. * P < 0.05

    Techniques Used: In Vivo

    Administration of PNSC928 significantly improve the inflammatory outcomes of ARDS mice. (A) A schematic representation illustrating PNSC928 administration. (B-G) Serum concentrations of proinflammatory cytokines by ELISA assays. (B) IL-1β, (C) IL-6, (D) IL-15, (E) IL-18, (F) TNF-α, and (G) IFN-γ. (H ) Body weights of mice measured at 0, 1, and 2 days. (I) pO 2 levels in mice measured at 0, 1, and 2 days. (J) Effects of PNSC928 on the expression levels of IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG. (K) Effects of PNSC928 on the expression levels of S100A8, CtBP2, ICAM1, SPP1, FBN1, and SPSB1. (L) Representative H&E staining images of lung from control, ARDS, PNSC928 groups of mice. Bars = 100 μm. (M) Quantification of histological scores. Images in (L) were quantified. n = 3 for each experiment. ns: no significant difference. * P < 0.05; ** P < 0.01; *** P < 0.001
    Figure Legend Snippet: Administration of PNSC928 significantly improve the inflammatory outcomes of ARDS mice. (A) A schematic representation illustrating PNSC928 administration. (B-G) Serum concentrations of proinflammatory cytokines by ELISA assays. (B) IL-1β, (C) IL-6, (D) IL-15, (E) IL-18, (F) TNF-α, and (G) IFN-γ. (H ) Body weights of mice measured at 0, 1, and 2 days. (I) pO 2 levels in mice measured at 0, 1, and 2 days. (J) Effects of PNSC928 on the expression levels of IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG. (K) Effects of PNSC928 on the expression levels of S100A8, CtBP2, ICAM1, SPP1, FBN1, and SPSB1. (L) Representative H&E staining images of lung from control, ARDS, PNSC928 groups of mice. Bars = 100 μm. (M) Quantification of histological scores. Images in (L) were quantified. n = 3 for each experiment. ns: no significant difference. * P < 0.05; ** P < 0.01; *** P < 0.001

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing, Staining, Control

    A schematic model of targeting CtBP2-p300 by PNSC928 to suppress the expression of proinflammatory cytokine genes and improve ARDS outcomes. (A) This schematic model illustrates the role of the CtBP2-p300-NF-κB complex in the activation of proinflammatory cytokine genes. CtBP2 forms a transcriptional complex with p300 and NF-κB subunits, leading to the activation of proinflammatory cytokine genes (IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG). The induction of these proinflammatory cytokines promotes the inflammatory response, contributing to the pathogenesis of ARDS. (B) This schematic model demonstrates the mechanism of action of PNSC928 in targeting the CtBP2-p300 complex. PNSC928 specifically disrupts the interaction between CtBP2 and p300, effectively suppressing the expression of proinflammatory cytokine genes. This intervention ultimately leads to improved outcomes in ARDS by mitigating the inflammatory response
    Figure Legend Snippet: A schematic model of targeting CtBP2-p300 by PNSC928 to suppress the expression of proinflammatory cytokine genes and improve ARDS outcomes. (A) This schematic model illustrates the role of the CtBP2-p300-NF-κB complex in the activation of proinflammatory cytokine genes. CtBP2 forms a transcriptional complex with p300 and NF-κB subunits, leading to the activation of proinflammatory cytokine genes (IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG). The induction of these proinflammatory cytokines promotes the inflammatory response, contributing to the pathogenesis of ARDS. (B) This schematic model demonstrates the mechanism of action of PNSC928 in targeting the CtBP2-p300 complex. PNSC928 specifically disrupts the interaction between CtBP2 and p300, effectively suppressing the expression of proinflammatory cytokine genes. This intervention ultimately leads to improved outcomes in ARDS by mitigating the inflammatory response

    Techniques Used: Expressing, Activation Assay



    Similar Products

    ards nsc95397  (MedChemExpress)
    93
    MedChemExpress ards nsc95397
    Proinflammatory cytokine genes were predominately upregulated in <t>ARDS</t> mice. (A) Experimental design: RNA-Seq analysis to identify differentially expressed genes (DGEs) in ARDS mice. (B) Volcano plot displaying RNA-Seq results. (C) Heatmap of top 20 upregulated genes and top 10 downregulated genes in ARDS lung tissues. (D) Biological processes of DGEs revealed by gene ontology (GO) analysis. (E and F) Verification of 12 DGEs by RT-qPCR analysis ( n = 3). (E) IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG. (F) S100A8, CtBP2, ICAM1, SPP1, FBN1, and SPSB1. ** P < 0.01; *** P < 0.001
    Ards Nsc95397, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ards nsc95397/product/MedChemExpress
    Average 93 stars, based on 1 article reviews
    ards nsc95397 - by Bioz Stars, 2026-03
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    Proinflammatory cytokine genes were predominately upregulated in ARDS mice. (A) Experimental design: RNA-Seq analysis to identify differentially expressed genes (DGEs) in ARDS mice. (B) Volcano plot displaying RNA-Seq results. (C) Heatmap of top 20 upregulated genes and top 10 downregulated genes in ARDS lung tissues. (D) Biological processes of DGEs revealed by gene ontology (GO) analysis. (E and F) Verification of 12 DGEs by RT-qPCR analysis ( n = 3). (E) IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG. (F) S100A8, CtBP2, ICAM1, SPP1, FBN1, and SPSB1. ** P < 0.01; *** P < 0.001

    Journal: Biology Direct

    Article Title: PNSC928, a plant-derived compound, specifically disrupts CtBP2-p300 interaction and reduces inflammation in mice with acute respiratory distress syndrome

    doi: 10.1186/s13062-024-00491-0

    Figure Lengend Snippet: Proinflammatory cytokine genes were predominately upregulated in ARDS mice. (A) Experimental design: RNA-Seq analysis to identify differentially expressed genes (DGEs) in ARDS mice. (B) Volcano plot displaying RNA-Seq results. (C) Heatmap of top 20 upregulated genes and top 10 downregulated genes in ARDS lung tissues. (D) Biological processes of DGEs revealed by gene ontology (GO) analysis. (E and F) Verification of 12 DGEs by RT-qPCR analysis ( n = 3). (E) IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG. (F) S100A8, CtBP2, ICAM1, SPP1, FBN1, and SPSB1. ** P < 0.01; *** P < 0.001

    Article Snippet: To assess the impact of CtBP2, p300, NF-κB inhibitors, and PNSC928 on ARDS progression, mice were further categorized post-4 h LPS administration into different groups: ARDS, ARDS + MTOB (700 mg/kg; MedChemExpress; Monmouth Junction, NJ; #HY-135,046), ARDS + NSC95397 (1.5 mg/kg; MedChemExpress; #HY-108,543), ARDS + C646 (10 mg/kg; MedChemExpress; #HY-13,823), ARDS + A-485 (50 mg/kg; MedChemExpress; #HY-107,455), ARDS + TPCA1 (10 mg/kg; MedChemExpress; #HY-10,074), ARDS + BOT64 (50 mg/kg; MedChemExpress; #HY-136,741), and ARDS + PNSC928 (20 mg/kg).

    Techniques: RNA Sequencing Assay, Quantitative RT-PCR

    Inhibitors of CtBP2, p300, and NF-κB exhibited cytotoxicity in vivo. C57BL/6 mice were administrated with MTOB (400 and 800 mg/kg), NSC95397 (2 and 4 mg/kg), C646 (5 and 10 mg/kg), A-485 (40 and 80 mg/kg), TPCA1 (10 and 20 mg/kg), BOT64 (30 and 60 mg/kg) for a duration of 6 days ( n = 10 for each group). (A-F) Body weights were measured every two days. (G-K) Serum concentrations of different groups of mice. (G) IL-1β, (H) IL-6, (I) IL-15, (J) IL-18, and (K) TNF-α. * P < 0.05

    Journal: Biology Direct

    Article Title: PNSC928, a plant-derived compound, specifically disrupts CtBP2-p300 interaction and reduces inflammation in mice with acute respiratory distress syndrome

    doi: 10.1186/s13062-024-00491-0

    Figure Lengend Snippet: Inhibitors of CtBP2, p300, and NF-κB exhibited cytotoxicity in vivo. C57BL/6 mice were administrated with MTOB (400 and 800 mg/kg), NSC95397 (2 and 4 mg/kg), C646 (5 and 10 mg/kg), A-485 (40 and 80 mg/kg), TPCA1 (10 and 20 mg/kg), BOT64 (30 and 60 mg/kg) for a duration of 6 days ( n = 10 for each group). (A-F) Body weights were measured every two days. (G-K) Serum concentrations of different groups of mice. (G) IL-1β, (H) IL-6, (I) IL-15, (J) IL-18, and (K) TNF-α. * P < 0.05

    Article Snippet: To assess the impact of CtBP2, p300, NF-κB inhibitors, and PNSC928 on ARDS progression, mice were further categorized post-4 h LPS administration into different groups: ARDS, ARDS + MTOB (700 mg/kg; MedChemExpress; Monmouth Junction, NJ; #HY-135,046), ARDS + NSC95397 (1.5 mg/kg; MedChemExpress; #HY-108,543), ARDS + C646 (10 mg/kg; MedChemExpress; #HY-13,823), ARDS + A-485 (50 mg/kg; MedChemExpress; #HY-107,455), ARDS + TPCA1 (10 mg/kg; MedChemExpress; #HY-10,074), ARDS + BOT64 (50 mg/kg; MedChemExpress; #HY-136,741), and ARDS + PNSC928 (20 mg/kg).

    Techniques: In Vivo

    Administration of PNSC928 significantly improve the inflammatory outcomes of ARDS mice. (A) A schematic representation illustrating PNSC928 administration. (B-G) Serum concentrations of proinflammatory cytokines by ELISA assays. (B) IL-1β, (C) IL-6, (D) IL-15, (E) IL-18, (F) TNF-α, and (G) IFN-γ. (H ) Body weights of mice measured at 0, 1, and 2 days. (I) pO 2 levels in mice measured at 0, 1, and 2 days. (J) Effects of PNSC928 on the expression levels of IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG. (K) Effects of PNSC928 on the expression levels of S100A8, CtBP2, ICAM1, SPP1, FBN1, and SPSB1. (L) Representative H&E staining images of lung from control, ARDS, PNSC928 groups of mice. Bars = 100 μm. (M) Quantification of histological scores. Images in (L) were quantified. n = 3 for each experiment. ns: no significant difference. * P < 0.05; ** P < 0.01; *** P < 0.001

    Journal: Biology Direct

    Article Title: PNSC928, a plant-derived compound, specifically disrupts CtBP2-p300 interaction and reduces inflammation in mice with acute respiratory distress syndrome

    doi: 10.1186/s13062-024-00491-0

    Figure Lengend Snippet: Administration of PNSC928 significantly improve the inflammatory outcomes of ARDS mice. (A) A schematic representation illustrating PNSC928 administration. (B-G) Serum concentrations of proinflammatory cytokines by ELISA assays. (B) IL-1β, (C) IL-6, (D) IL-15, (E) IL-18, (F) TNF-α, and (G) IFN-γ. (H ) Body weights of mice measured at 0, 1, and 2 days. (I) pO 2 levels in mice measured at 0, 1, and 2 days. (J) Effects of PNSC928 on the expression levels of IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG. (K) Effects of PNSC928 on the expression levels of S100A8, CtBP2, ICAM1, SPP1, FBN1, and SPSB1. (L) Representative H&E staining images of lung from control, ARDS, PNSC928 groups of mice. Bars = 100 μm. (M) Quantification of histological scores. Images in (L) were quantified. n = 3 for each experiment. ns: no significant difference. * P < 0.05; ** P < 0.01; *** P < 0.001

    Article Snippet: To assess the impact of CtBP2, p300, NF-κB inhibitors, and PNSC928 on ARDS progression, mice were further categorized post-4 h LPS administration into different groups: ARDS, ARDS + MTOB (700 mg/kg; MedChemExpress; Monmouth Junction, NJ; #HY-135,046), ARDS + NSC95397 (1.5 mg/kg; MedChemExpress; #HY-108,543), ARDS + C646 (10 mg/kg; MedChemExpress; #HY-13,823), ARDS + A-485 (50 mg/kg; MedChemExpress; #HY-107,455), ARDS + TPCA1 (10 mg/kg; MedChemExpress; #HY-10,074), ARDS + BOT64 (50 mg/kg; MedChemExpress; #HY-136,741), and ARDS + PNSC928 (20 mg/kg).

    Techniques: Enzyme-linked Immunosorbent Assay, Expressing, Staining, Control

    A schematic model of targeting CtBP2-p300 by PNSC928 to suppress the expression of proinflammatory cytokine genes and improve ARDS outcomes. (A) This schematic model illustrates the role of the CtBP2-p300-NF-κB complex in the activation of proinflammatory cytokine genes. CtBP2 forms a transcriptional complex with p300 and NF-κB subunits, leading to the activation of proinflammatory cytokine genes (IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG). The induction of these proinflammatory cytokines promotes the inflammatory response, contributing to the pathogenesis of ARDS. (B) This schematic model demonstrates the mechanism of action of PNSC928 in targeting the CtBP2-p300 complex. PNSC928 specifically disrupts the interaction between CtBP2 and p300, effectively suppressing the expression of proinflammatory cytokine genes. This intervention ultimately leads to improved outcomes in ARDS by mitigating the inflammatory response

    Journal: Biology Direct

    Article Title: PNSC928, a plant-derived compound, specifically disrupts CtBP2-p300 interaction and reduces inflammation in mice with acute respiratory distress syndrome

    doi: 10.1186/s13062-024-00491-0

    Figure Lengend Snippet: A schematic model of targeting CtBP2-p300 by PNSC928 to suppress the expression of proinflammatory cytokine genes and improve ARDS outcomes. (A) This schematic model illustrates the role of the CtBP2-p300-NF-κB complex in the activation of proinflammatory cytokine genes. CtBP2 forms a transcriptional complex with p300 and NF-κB subunits, leading to the activation of proinflammatory cytokine genes (IL-1B, IL-6, IL-15, IL-18, TNFA, and IFNG). The induction of these proinflammatory cytokines promotes the inflammatory response, contributing to the pathogenesis of ARDS. (B) This schematic model demonstrates the mechanism of action of PNSC928 in targeting the CtBP2-p300 complex. PNSC928 specifically disrupts the interaction between CtBP2 and p300, effectively suppressing the expression of proinflammatory cytokine genes. This intervention ultimately leads to improved outcomes in ARDS by mitigating the inflammatory response

    Article Snippet: To assess the impact of CtBP2, p300, NF-κB inhibitors, and PNSC928 on ARDS progression, mice were further categorized post-4 h LPS administration into different groups: ARDS, ARDS + MTOB (700 mg/kg; MedChemExpress; Monmouth Junction, NJ; #HY-135,046), ARDS + NSC95397 (1.5 mg/kg; MedChemExpress; #HY-108,543), ARDS + C646 (10 mg/kg; MedChemExpress; #HY-13,823), ARDS + A-485 (50 mg/kg; MedChemExpress; #HY-107,455), ARDS + TPCA1 (10 mg/kg; MedChemExpress; #HY-10,074), ARDS + BOT64 (50 mg/kg; MedChemExpress; #HY-136,741), and ARDS + PNSC928 (20 mg/kg).

    Techniques: Expressing, Activation Assay