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s100a9 inhibitor experiment  (MedChemExpress)


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    MedChemExpress s100a9 inhibitor experiment
    The loss of FGF20 increases colonic <t>S100A9</t> expression in DSS-induced mice. ( A ) Heat maps of differentially expressed proteins in the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Volcano diagram of proteomic analysis in FGF20 KO and WT mice with colitis. ( C ) Relative expression data of S100A9 in FGF20 KO and WT mice with or without colitis (n = 4). ( D, E ) The expression of S100A9 in the colonic tissue of each group of mice was tested by Western blot (n = 3) and immunohistochemistry (n = 4). Data are represented as mean ± SEM. Scale bar, 50 μm. ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.
    S100a9 Inhibitor Experiment, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 53 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/s100a9 inhibitor experiment/product/MedChemExpress
    Average 95 stars, based on 53 article reviews
    s100a9 inhibitor experiment - by Bioz Stars, 2026-02
    95/100 stars

    Images

    1) Product Images from "Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner"

    Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    doi: 10.1016/j.jcmgh.2025.101486

    The loss of FGF20 increases colonic S100A9 expression in DSS-induced mice. ( A ) Heat maps of differentially expressed proteins in the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Volcano diagram of proteomic analysis in FGF20 KO and WT mice with colitis. ( C ) Relative expression data of S100A9 in FGF20 KO and WT mice with or without colitis (n = 4). ( D, E ) The expression of S100A9 in the colonic tissue of each group of mice was tested by Western blot (n = 3) and immunohistochemistry (n = 4). Data are represented as mean ± SEM. Scale bar, 50 μm. ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.
    Figure Legend Snippet: The loss of FGF20 increases colonic S100A9 expression in DSS-induced mice. ( A ) Heat maps of differentially expressed proteins in the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Volcano diagram of proteomic analysis in FGF20 KO and WT mice with colitis. ( C ) Relative expression data of S100A9 in FGF20 KO and WT mice with or without colitis (n = 4). ( D, E ) The expression of S100A9 in the colonic tissue of each group of mice was tested by Western blot (n = 3) and immunohistochemistry (n = 4). Data are represented as mean ± SEM. Scale bar, 50 μm. ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

    Techniques Used: Expressing, Western Blot, Immunohistochemistry

    Inhibition of S100A9 protects against colitis in FGF20 KO mice. Eight-week-old male FGF20 KO mice and WT littermates were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. In the meanwhile, paquinimod (10 mg/kg) was injected via the intraperitoneal route for 10 days. ( A, B ) Body weight and colon length of FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. ( C ) Histologic morphology of FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Top , H&E staining; bottom , PAS staining. Scale bar, 100 μm and 50 μm. ( D ) Immunoblot analysis of colonic IL6 and iNOS in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗∗ P < .001.
    Figure Legend Snippet: Inhibition of S100A9 protects against colitis in FGF20 KO mice. Eight-week-old male FGF20 KO mice and WT littermates were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. In the meanwhile, paquinimod (10 mg/kg) was injected via the intraperitoneal route for 10 days. ( A, B ) Body weight and colon length of FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. ( C ) Histologic morphology of FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Top , H&E staining; bottom , PAS staining. Scale bar, 100 μm and 50 μm. ( D ) Immunoblot analysis of colonic IL6 and iNOS in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗∗ P < .001.

    Techniques Used: Inhibition, Injection, Staining, Western Blot

    AAV-S100A9 attenuates the protective effects of FGF20-overexpression against DSS-induced colitis. Six-week-old male WT mice were treated with AAV-FGF20, AAV-S100A9, or AAV-GFP by tail vein injection. After 4 weeks of AAV injection, all mice were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. ( A ) The expression of S100A9 after AAV-S100A9 treatment was determined by Western blot (n = 6). ( B, C ) Body weights and colon length of AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not were measured. ( D ) Histologic morphology of AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Top , H&E staining; bottom , PAS staining. Scale bar, 100 μm and 50 μm. ( E ) Immunoblot analysis of colonic IL6 and iNOS in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.
    Figure Legend Snippet: AAV-S100A9 attenuates the protective effects of FGF20-overexpression against DSS-induced colitis. Six-week-old male WT mice were treated with AAV-FGF20, AAV-S100A9, or AAV-GFP by tail vein injection. After 4 weeks of AAV injection, all mice were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. ( A ) The expression of S100A9 after AAV-S100A9 treatment was determined by Western blot (n = 6). ( B, C ) Body weights and colon length of AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not were measured. ( D ) Histologic morphology of AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Top , H&E staining; bottom , PAS staining. Scale bar, 100 μm and 50 μm. ( E ) Immunoblot analysis of colonic IL6 and iNOS in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

    Techniques Used: Over Expression, Injection, Expressing, Western Blot, Staining

    Inhibition of S100A9 mitigated the deterioration of FGF20 KO on intestinal barrier function in DSS-induced colitis. Eight-week-old male FGF20 KO mice and WT littermates were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. In the meanwhile, paquinimod (10 mg/kg) was injected via the intraperitoneal route for 10 days. ( A ) Western blot and quantitation of colonic ZO-2, occludin, and claudin 1 expression in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). ( B ) Representative fluorescence images of Ki67, and the percentage of Ki67-positive cells in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Scale bar, 50 μm (n ≥ 5). ( C ) Immunoblot analysis of colonic Bax and Bcl-2 expression in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗∗ P < .001.
    Figure Legend Snippet: Inhibition of S100A9 mitigated the deterioration of FGF20 KO on intestinal barrier function in DSS-induced colitis. Eight-week-old male FGF20 KO mice and WT littermates were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. In the meanwhile, paquinimod (10 mg/kg) was injected via the intraperitoneal route for 10 days. ( A ) Western blot and quantitation of colonic ZO-2, occludin, and claudin 1 expression in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). ( B ) Representative fluorescence images of Ki67, and the percentage of Ki67-positive cells in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Scale bar, 50 μm (n ≥ 5). ( C ) Immunoblot analysis of colonic Bax and Bcl-2 expression in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗∗ P < .001.

    Techniques Used: Inhibition, Injection, Western Blot, Quantitation Assay, Expressing, Fluorescence

    FGF20 regulates claudin-1 through S100A9 in DSS-induced colitis mice. ( A ) Representative fluorescence images of colonic claudin-1 from FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. ( B ) Representative fluorescence images of colonic claudin-1 from AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Scale bar, 50 μm.
    Figure Legend Snippet: FGF20 regulates claudin-1 through S100A9 in DSS-induced colitis mice. ( A ) Representative fluorescence images of colonic claudin-1 from FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. ( B ) Representative fluorescence images of colonic claudin-1 from AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Scale bar, 50 μm.

    Techniques Used: Fluorescence

    AAV-S100A9 abolished the protect effects of FGF20 overexpression on intestinal barrier function in DSS-induced colitis. Six-week-old male WT mice were treated with AAV-FGF20, AAV-S100A9, or AAV-GFP by tail vein injection. After 4 weeks of AAV injection, all mice were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. ( A ) Western blot and quantitation of colonic ZO-2, occludin, and claudin-1 expression in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). ( B ) Representative fluorescence images of Ki67, and the percentage of Ki67-positive cells in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n ≥ 5), Scale bar, 50 μm. ( C ) The expression of level of Bax and Bcl-2 in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not, were detected by Western blot (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001. n.s., no significance.
    Figure Legend Snippet: AAV-S100A9 abolished the protect effects of FGF20 overexpression on intestinal barrier function in DSS-induced colitis. Six-week-old male WT mice were treated with AAV-FGF20, AAV-S100A9, or AAV-GFP by tail vein injection. After 4 weeks of AAV injection, all mice were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. ( A ) Western blot and quantitation of colonic ZO-2, occludin, and claudin-1 expression in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). ( B ) Representative fluorescence images of Ki67, and the percentage of Ki67-positive cells in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n ≥ 5), Scale bar, 50 μm. ( C ) The expression of level of Bax and Bcl-2 in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not, were detected by Western blot (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001. n.s., no significance.

    Techniques Used: Over Expression, Injection, Western Blot, Quantitation Assay, Expressing, Fluorescence

    The inhibition of FGF20 on M1-like macrophage polarization in DSS-induced colitis was S100A9-dependent. ( A, B ) mRNA expression levels of macrophage M1 ( IL-6 , TNF-α , IL-1β , and MCP-1 ) and M2 ( IL-10 , Arg-1, Fizz1 , and Ym1 ) polarization-related gene in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle, were quantitatively determined by quantitative PCR (n ≥ 4). ( C, D ) mRNA expression levels of macrophage M1 ( IL-6 , TNF-α , IL-1β , and MCP-1 ) and M2 ( IL-10 , Arg-1, Fizz1 , and Ym1 ) polarization-related gene in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not, were quantitatively determined by quantitative PCR (n ≥ 4). ( E ) Representative images of immunofluorescence staining of colon sections from FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Scale bar, 50 μm. ( F ) Representative images of immunofluorescence staining of colon sections from AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Scale bar, 50 μm. Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001. n.s., no significance.
    Figure Legend Snippet: The inhibition of FGF20 on M1-like macrophage polarization in DSS-induced colitis was S100A9-dependent. ( A, B ) mRNA expression levels of macrophage M1 ( IL-6 , TNF-α , IL-1β , and MCP-1 ) and M2 ( IL-10 , Arg-1, Fizz1 , and Ym1 ) polarization-related gene in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle, were quantitatively determined by quantitative PCR (n ≥ 4). ( C, D ) mRNA expression levels of macrophage M1 ( IL-6 , TNF-α , IL-1β , and MCP-1 ) and M2 ( IL-10 , Arg-1, Fizz1 , and Ym1 ) polarization-related gene in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not, were quantitatively determined by quantitative PCR (n ≥ 4). ( E ) Representative images of immunofluorescence staining of colon sections from FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Scale bar, 50 μm. ( F ) Representative images of immunofluorescence staining of colon sections from AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Scale bar, 50 μm. Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001. n.s., no significance.

    Techniques Used: Inhibition, Expressing, Real-time Polymerase Chain Reaction, Immunofluorescence, Staining

    FGF20 inhibits NF-κB pathway through S100A9 in DDS-induced mice. ( A ) KEGG Enrichment Analysis of proteomics data from the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα from FGF20 KO and WT mice with or without colitis (n = 6). ( C ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in AAV-FGF20- or AAV-GFP-treated mice with or without colitis. ( D ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). ( E ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.
    Figure Legend Snippet: FGF20 inhibits NF-κB pathway through S100A9 in DDS-induced mice. ( A ) KEGG Enrichment Analysis of proteomics data from the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα from FGF20 KO and WT mice with or without colitis (n = 6). ( C ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in AAV-FGF20- or AAV-GFP-treated mice with or without colitis. ( D ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). ( E ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

    Techniques Used: Western Blot

    FGF20 inhibits M1-like macrophage polarization in NF-κB-dependent manner in vitro. Primary peritoneal macrophages were isolated from WT mice and FGF20 KO mice and used for subsequent in vitro experiments. ( A ) Immunoblot analysis of expression of iNOS, TNF-α, IL6, S100A9, p-P65, P65, p-IκBα, and IκBα in LPS-stimulated primary peritoneal macrophages, treated with or without BAY11-7082 (n = 3). ( B ) Representative immunofluorescence images and its fluorescence densities of LPS-stimulated primary peritoneal macrophages, treated with or without BAY11-7082 (n = 6). Data are represented as mean ± SEM; ∗∗ P < .01, ∗∗∗ P < .001.
    Figure Legend Snippet: FGF20 inhibits M1-like macrophage polarization in NF-κB-dependent manner in vitro. Primary peritoneal macrophages were isolated from WT mice and FGF20 KO mice and used for subsequent in vitro experiments. ( A ) Immunoblot analysis of expression of iNOS, TNF-α, IL6, S100A9, p-P65, P65, p-IκBα, and IκBα in LPS-stimulated primary peritoneal macrophages, treated with or without BAY11-7082 (n = 3). ( B ) Representative immunofluorescence images and its fluorescence densities of LPS-stimulated primary peritoneal macrophages, treated with or without BAY11-7082 (n = 6). Data are represented as mean ± SEM; ∗∗ P < .01, ∗∗∗ P < .001.

    Techniques Used: In Vitro, Isolation, Western Blot, Expressing, Immunofluorescence, Fluorescence



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    The loss of FGF20 increases colonic <t>S100A9</t> expression in DSS-induced mice. ( A ) Heat maps of differentially expressed proteins in the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Volcano diagram of proteomic analysis in FGF20 KO and WT mice with colitis. ( C ) Relative expression data of S100A9 in FGF20 KO and WT mice with or without colitis (n = 4). ( D, E ) The expression of S100A9 in the colonic tissue of each group of mice was tested by Western blot (n = 3) and immunohistochemistry (n = 4). Data are represented as mean ± SEM. Scale bar, 50 μm. ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.
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    The loss of FGF20 increases colonic <t>S100A9</t> expression in DSS-induced mice. ( A ) Heat maps of differentially expressed proteins in the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Volcano diagram of proteomic analysis in FGF20 KO and WT mice with colitis. ( C ) Relative expression data of S100A9 in FGF20 KO and WT mice with or without colitis (n = 4). ( D, E ) The expression of S100A9 in the colonic tissue of each group of mice was tested by Western blot (n = 3) and immunohistochemistry (n = 4). Data are represented as mean ± SEM. Scale bar, 50 μm. ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.
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    The loss of FGF20 increases colonic S100A9 expression in DSS-induced mice. ( A ) Heat maps of differentially expressed proteins in the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Volcano diagram of proteomic analysis in FGF20 KO and WT mice with colitis. ( C ) Relative expression data of S100A9 in FGF20 KO and WT mice with or without colitis (n = 4). ( D, E ) The expression of S100A9 in the colonic tissue of each group of mice was tested by Western blot (n = 3) and immunohistochemistry (n = 4). Data are represented as mean ± SEM. Scale bar, 50 μm. ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

    doi: 10.1016/j.jcmgh.2025.101486

    Figure Lengend Snippet: The loss of FGF20 increases colonic S100A9 expression in DSS-induced mice. ( A ) Heat maps of differentially expressed proteins in the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Volcano diagram of proteomic analysis in FGF20 KO and WT mice with colitis. ( C ) Relative expression data of S100A9 in FGF20 KO and WT mice with or without colitis (n = 4). ( D, E ) The expression of S100A9 in the colonic tissue of each group of mice was tested by Western blot (n = 3) and immunohistochemistry (n = 4). Data are represented as mean ± SEM. Scale bar, 50 μm. ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

    Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

    Techniques: Expressing, Western Blot, Immunohistochemistry

    Inhibition of S100A9 protects against colitis in FGF20 KO mice. Eight-week-old male FGF20 KO mice and WT littermates were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. In the meanwhile, paquinimod (10 mg/kg) was injected via the intraperitoneal route for 10 days. ( A, B ) Body weight and colon length of FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. ( C ) Histologic morphology of FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Top , H&E staining; bottom , PAS staining. Scale bar, 100 μm and 50 μm. ( D ) Immunoblot analysis of colonic IL6 and iNOS in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗∗ P < .001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

    doi: 10.1016/j.jcmgh.2025.101486

    Figure Lengend Snippet: Inhibition of S100A9 protects against colitis in FGF20 KO mice. Eight-week-old male FGF20 KO mice and WT littermates were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. In the meanwhile, paquinimod (10 mg/kg) was injected via the intraperitoneal route for 10 days. ( A, B ) Body weight and colon length of FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. ( C ) Histologic morphology of FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Top , H&E staining; bottom , PAS staining. Scale bar, 100 μm and 50 μm. ( D ) Immunoblot analysis of colonic IL6 and iNOS in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗∗ P < .001.

    Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

    Techniques: Inhibition, Injection, Staining, Western Blot

    AAV-S100A9 attenuates the protective effects of FGF20-overexpression against DSS-induced colitis. Six-week-old male WT mice were treated with AAV-FGF20, AAV-S100A9, or AAV-GFP by tail vein injection. After 4 weeks of AAV injection, all mice were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. ( A ) The expression of S100A9 after AAV-S100A9 treatment was determined by Western blot (n = 6). ( B, C ) Body weights and colon length of AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not were measured. ( D ) Histologic morphology of AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Top , H&E staining; bottom , PAS staining. Scale bar, 100 μm and 50 μm. ( E ) Immunoblot analysis of colonic IL6 and iNOS in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

    doi: 10.1016/j.jcmgh.2025.101486

    Figure Lengend Snippet: AAV-S100A9 attenuates the protective effects of FGF20-overexpression against DSS-induced colitis. Six-week-old male WT mice were treated with AAV-FGF20, AAV-S100A9, or AAV-GFP by tail vein injection. After 4 weeks of AAV injection, all mice were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. ( A ) The expression of S100A9 after AAV-S100A9 treatment was determined by Western blot (n = 6). ( B, C ) Body weights and colon length of AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not were measured. ( D ) Histologic morphology of AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Top , H&E staining; bottom , PAS staining. Scale bar, 100 μm and 50 μm. ( E ) Immunoblot analysis of colonic IL6 and iNOS in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

    Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

    Techniques: Over Expression, Injection, Expressing, Western Blot, Staining

    Inhibition of S100A9 mitigated the deterioration of FGF20 KO on intestinal barrier function in DSS-induced colitis. Eight-week-old male FGF20 KO mice and WT littermates were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. In the meanwhile, paquinimod (10 mg/kg) was injected via the intraperitoneal route for 10 days. ( A ) Western blot and quantitation of colonic ZO-2, occludin, and claudin 1 expression in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). ( B ) Representative fluorescence images of Ki67, and the percentage of Ki67-positive cells in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Scale bar, 50 μm (n ≥ 5). ( C ) Immunoblot analysis of colonic Bax and Bcl-2 expression in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗∗ P < .001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

    doi: 10.1016/j.jcmgh.2025.101486

    Figure Lengend Snippet: Inhibition of S100A9 mitigated the deterioration of FGF20 KO on intestinal barrier function in DSS-induced colitis. Eight-week-old male FGF20 KO mice and WT littermates were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. In the meanwhile, paquinimod (10 mg/kg) was injected via the intraperitoneal route for 10 days. ( A ) Western blot and quantitation of colonic ZO-2, occludin, and claudin 1 expression in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). ( B ) Representative fluorescence images of Ki67, and the percentage of Ki67-positive cells in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Scale bar, 50 μm (n ≥ 5). ( C ) Immunoblot analysis of colonic Bax and Bcl-2 expression in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗∗ P < .001.

    Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

    Techniques: Inhibition, Injection, Western Blot, Quantitation Assay, Expressing, Fluorescence

    FGF20 regulates claudin-1 through S100A9 in DSS-induced colitis mice. ( A ) Representative fluorescence images of colonic claudin-1 from FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. ( B ) Representative fluorescence images of colonic claudin-1 from AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Scale bar, 50 μm.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

    doi: 10.1016/j.jcmgh.2025.101486

    Figure Lengend Snippet: FGF20 regulates claudin-1 through S100A9 in DSS-induced colitis mice. ( A ) Representative fluorescence images of colonic claudin-1 from FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. ( B ) Representative fluorescence images of colonic claudin-1 from AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Scale bar, 50 μm.

    Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

    Techniques: Fluorescence

    AAV-S100A9 abolished the protect effects of FGF20 overexpression on intestinal barrier function in DSS-induced colitis. Six-week-old male WT mice were treated with AAV-FGF20, AAV-S100A9, or AAV-GFP by tail vein injection. After 4 weeks of AAV injection, all mice were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. ( A ) Western blot and quantitation of colonic ZO-2, occludin, and claudin-1 expression in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). ( B ) Representative fluorescence images of Ki67, and the percentage of Ki67-positive cells in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n ≥ 5), Scale bar, 50 μm. ( C ) The expression of level of Bax and Bcl-2 in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not, were detected by Western blot (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001. n.s., no significance.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

    doi: 10.1016/j.jcmgh.2025.101486

    Figure Lengend Snippet: AAV-S100A9 abolished the protect effects of FGF20 overexpression on intestinal barrier function in DSS-induced colitis. Six-week-old male WT mice were treated with AAV-FGF20, AAV-S100A9, or AAV-GFP by tail vein injection. After 4 weeks of AAV injection, all mice were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. ( A ) Western blot and quantitation of colonic ZO-2, occludin, and claudin-1 expression in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). ( B ) Representative fluorescence images of Ki67, and the percentage of Ki67-positive cells in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n ≥ 5), Scale bar, 50 μm. ( C ) The expression of level of Bax and Bcl-2 in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not, were detected by Western blot (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001. n.s., no significance.

    Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

    Techniques: Over Expression, Injection, Western Blot, Quantitation Assay, Expressing, Fluorescence

    The inhibition of FGF20 on M1-like macrophage polarization in DSS-induced colitis was S100A9-dependent. ( A, B ) mRNA expression levels of macrophage M1 ( IL-6 , TNF-α , IL-1β , and MCP-1 ) and M2 ( IL-10 , Arg-1, Fizz1 , and Ym1 ) polarization-related gene in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle, were quantitatively determined by quantitative PCR (n ≥ 4). ( C, D ) mRNA expression levels of macrophage M1 ( IL-6 , TNF-α , IL-1β , and MCP-1 ) and M2 ( IL-10 , Arg-1, Fizz1 , and Ym1 ) polarization-related gene in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not, were quantitatively determined by quantitative PCR (n ≥ 4). ( E ) Representative images of immunofluorescence staining of colon sections from FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Scale bar, 50 μm. ( F ) Representative images of immunofluorescence staining of colon sections from AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Scale bar, 50 μm. Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001. n.s., no significance.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

    doi: 10.1016/j.jcmgh.2025.101486

    Figure Lengend Snippet: The inhibition of FGF20 on M1-like macrophage polarization in DSS-induced colitis was S100A9-dependent. ( A, B ) mRNA expression levels of macrophage M1 ( IL-6 , TNF-α , IL-1β , and MCP-1 ) and M2 ( IL-10 , Arg-1, Fizz1 , and Ym1 ) polarization-related gene in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle, were quantitatively determined by quantitative PCR (n ≥ 4). ( C, D ) mRNA expression levels of macrophage M1 ( IL-6 , TNF-α , IL-1β , and MCP-1 ) and M2 ( IL-10 , Arg-1, Fizz1 , and Ym1 ) polarization-related gene in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not, were quantitatively determined by quantitative PCR (n ≥ 4). ( E ) Representative images of immunofluorescence staining of colon sections from FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Scale bar, 50 μm. ( F ) Representative images of immunofluorescence staining of colon sections from AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Scale bar, 50 μm. Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001. n.s., no significance.

    Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

    Techniques: Inhibition, Expressing, Real-time Polymerase Chain Reaction, Immunofluorescence, Staining

    FGF20 inhibits NF-κB pathway through S100A9 in DDS-induced mice. ( A ) KEGG Enrichment Analysis of proteomics data from the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα from FGF20 KO and WT mice with or without colitis (n = 6). ( C ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in AAV-FGF20- or AAV-GFP-treated mice with or without colitis. ( D ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). ( E ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

    doi: 10.1016/j.jcmgh.2025.101486

    Figure Lengend Snippet: FGF20 inhibits NF-κB pathway through S100A9 in DDS-induced mice. ( A ) KEGG Enrichment Analysis of proteomics data from the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα from FGF20 KO and WT mice with or without colitis (n = 6). ( C ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in AAV-FGF20- or AAV-GFP-treated mice with or without colitis. ( D ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). ( E ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

    Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

    Techniques: Western Blot

    FGF20 inhibits M1-like macrophage polarization in NF-κB-dependent manner in vitro. Primary peritoneal macrophages were isolated from WT mice and FGF20 KO mice and used for subsequent in vitro experiments. ( A ) Immunoblot analysis of expression of iNOS, TNF-α, IL6, S100A9, p-P65, P65, p-IκBα, and IκBα in LPS-stimulated primary peritoneal macrophages, treated with or without BAY11-7082 (n = 3). ( B ) Representative immunofluorescence images and its fluorescence densities of LPS-stimulated primary peritoneal macrophages, treated with or without BAY11-7082 (n = 6). Data are represented as mean ± SEM; ∗∗ P < .01, ∗∗∗ P < .001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

    doi: 10.1016/j.jcmgh.2025.101486

    Figure Lengend Snippet: FGF20 inhibits M1-like macrophage polarization in NF-κB-dependent manner in vitro. Primary peritoneal macrophages were isolated from WT mice and FGF20 KO mice and used for subsequent in vitro experiments. ( A ) Immunoblot analysis of expression of iNOS, TNF-α, IL6, S100A9, p-P65, P65, p-IκBα, and IκBα in LPS-stimulated primary peritoneal macrophages, treated with or without BAY11-7082 (n = 3). ( B ) Representative immunofluorescence images and its fluorescence densities of LPS-stimulated primary peritoneal macrophages, treated with or without BAY11-7082 (n = 6). Data are represented as mean ± SEM; ∗∗ P < .01, ∗∗∗ P < .001.

    Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

    Techniques: In Vitro, Isolation, Western Blot, Expressing, Immunofluorescence, Fluorescence