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col3a1  (Proteintech)


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    Proteintech col3a1
    Gut microbiota partially mediates the protective effects of perinatal Ind and I3A exposure on hepatic fibrosis and ceramide metabolism. ( a ) Body weight monitored weekly in FMT recipients. Data are mean ± SEM, n = 5/group. ( b ) Histological examination of liver sections from FMT recipients by H&E, picrosirius red (PSR), and immunohistochemistry of <t>COL3A1</t> to quantify fibrosis. Representative images are shown from n = 5 mice/group. Magnification: 20×; scale bar: 100 μm. Quantification of PSR positive area ( c ) and COL3A1 ( d ). Data are mean ± SEM; n = 5/group. ∗p < 0.05 and ∗∗p < 0.01 vs. WD by one-way ANOVA with Dunnett's test. ( e ) Hepatic long-chain (LC) and very long-chain (VLC) ceramide levels by LC-MS. Data are mean ± SEM; n = 5/group.∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. Hepatic gene expression of ceramide synthesis genes ( f ), ceramide degradation genes ( g ), and Ahr and its canonical targets ( h ) by qPCR, normalised to Rn18s . Data are mean ± SEM; n = 5/group. ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. ( i ) Gene expression of tight junction genes in ileum from FMT recipients by qPCR, normalised to Rn18s . Data are mean ± SEM; n = 5/group. ∗p < 0.05 vs. WD by Kruskal–Wallis with Dunn's test.
    Col3a1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 510 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/col3a1/product/Proteintech
    Average 96 stars, based on 510 article reviews
    col3a1 - by Bioz Stars, 2026-02
    96/100 stars

    Images

    1) Product Images from "Reprogramming offspring liver health: maternal indole supplementation as a preventive strategy against MASLD"

    Article Title: Reprogramming offspring liver health: maternal indole supplementation as a preventive strategy against MASLD

    Journal: eBioMedicine

    doi: 10.1016/j.ebiom.2025.106098

    Gut microbiota partially mediates the protective effects of perinatal Ind and I3A exposure on hepatic fibrosis and ceramide metabolism. ( a ) Body weight monitored weekly in FMT recipients. Data are mean ± SEM, n = 5/group. ( b ) Histological examination of liver sections from FMT recipients by H&E, picrosirius red (PSR), and immunohistochemistry of COL3A1 to quantify fibrosis. Representative images are shown from n = 5 mice/group. Magnification: 20×; scale bar: 100 μm. Quantification of PSR positive area ( c ) and COL3A1 ( d ). Data are mean ± SEM; n = 5/group. ∗p < 0.05 and ∗∗p < 0.01 vs. WD by one-way ANOVA with Dunnett's test. ( e ) Hepatic long-chain (LC) and very long-chain (VLC) ceramide levels by LC-MS. Data are mean ± SEM; n = 5/group.∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. Hepatic gene expression of ceramide synthesis genes ( f ), ceramide degradation genes ( g ), and Ahr and its canonical targets ( h ) by qPCR, normalised to Rn18s . Data are mean ± SEM; n = 5/group. ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. ( i ) Gene expression of tight junction genes in ileum from FMT recipients by qPCR, normalised to Rn18s . Data are mean ± SEM; n = 5/group. ∗p < 0.05 vs. WD by Kruskal–Wallis with Dunn's test.
    Figure Legend Snippet: Gut microbiota partially mediates the protective effects of perinatal Ind and I3A exposure on hepatic fibrosis and ceramide metabolism. ( a ) Body weight monitored weekly in FMT recipients. Data are mean ± SEM, n = 5/group. ( b ) Histological examination of liver sections from FMT recipients by H&E, picrosirius red (PSR), and immunohistochemistry of COL3A1 to quantify fibrosis. Representative images are shown from n = 5 mice/group. Magnification: 20×; scale bar: 100 μm. Quantification of PSR positive area ( c ) and COL3A1 ( d ). Data are mean ± SEM; n = 5/group. ∗p < 0.05 and ∗∗p < 0.01 vs. WD by one-way ANOVA with Dunnett's test. ( e ) Hepatic long-chain (LC) and very long-chain (VLC) ceramide levels by LC-MS. Data are mean ± SEM; n = 5/group.∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. Hepatic gene expression of ceramide synthesis genes ( f ), ceramide degradation genes ( g ), and Ahr and its canonical targets ( h ) by qPCR, normalised to Rn18s . Data are mean ± SEM; n = 5/group. ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. ( i ) Gene expression of tight junction genes in ileum from FMT recipients by qPCR, normalised to Rn18s . Data are mean ± SEM; n = 5/group. ∗p < 0.05 vs. WD by Kruskal–Wallis with Dunn's test.

    Techniques Used: Immunohistochemistry, Liquid Chromatography with Mass Spectroscopy, Gene Expression



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    Image Search Results


    Gut microbiota partially mediates the protective effects of perinatal Ind and I3A exposure on hepatic fibrosis and ceramide metabolism. ( a ) Body weight monitored weekly in FMT recipients. Data are mean ± SEM, n = 5/group. ( b ) Histological examination of liver sections from FMT recipients by H&E, picrosirius red (PSR), and immunohistochemistry of COL3A1 to quantify fibrosis. Representative images are shown from n = 5 mice/group. Magnification: 20×; scale bar: 100 μm. Quantification of PSR positive area ( c ) and COL3A1 ( d ). Data are mean ± SEM; n = 5/group. ∗p < 0.05 and ∗∗p < 0.01 vs. WD by one-way ANOVA with Dunnett's test. ( e ) Hepatic long-chain (LC) and very long-chain (VLC) ceramide levels by LC-MS. Data are mean ± SEM; n = 5/group.∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. Hepatic gene expression of ceramide synthesis genes ( f ), ceramide degradation genes ( g ), and Ahr and its canonical targets ( h ) by qPCR, normalised to Rn18s . Data are mean ± SEM; n = 5/group. ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. ( i ) Gene expression of tight junction genes in ileum from FMT recipients by qPCR, normalised to Rn18s . Data are mean ± SEM; n = 5/group. ∗p < 0.05 vs. WD by Kruskal–Wallis with Dunn's test.

    Journal: eBioMedicine

    Article Title: Reprogramming offspring liver health: maternal indole supplementation as a preventive strategy against MASLD

    doi: 10.1016/j.ebiom.2025.106098

    Figure Lengend Snippet: Gut microbiota partially mediates the protective effects of perinatal Ind and I3A exposure on hepatic fibrosis and ceramide metabolism. ( a ) Body weight monitored weekly in FMT recipients. Data are mean ± SEM, n = 5/group. ( b ) Histological examination of liver sections from FMT recipients by H&E, picrosirius red (PSR), and immunohistochemistry of COL3A1 to quantify fibrosis. Representative images are shown from n = 5 mice/group. Magnification: 20×; scale bar: 100 μm. Quantification of PSR positive area ( c ) and COL3A1 ( d ). Data are mean ± SEM; n = 5/group. ∗p < 0.05 and ∗∗p < 0.01 vs. WD by one-way ANOVA with Dunnett's test. ( e ) Hepatic long-chain (LC) and very long-chain (VLC) ceramide levels by LC-MS. Data are mean ± SEM; n = 5/group.∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. Hepatic gene expression of ceramide synthesis genes ( f ), ceramide degradation genes ( g ), and Ahr and its canonical targets ( h ) by qPCR, normalised to Rn18s . Data are mean ± SEM; n = 5/group. ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. ( i ) Gene expression of tight junction genes in ileum from FMT recipients by qPCR, normalised to Rn18s . Data are mean ± SEM; n = 5/group. ∗p < 0.05 vs. WD by Kruskal–Wallis with Dunn's test.

    Article Snippet: Sections were incubated in 5% goat serum for 30 min, primary antibody COL1A1 (liver; 1:200; Cell Signalling Technologies [CST] Cat# 72026, RRID: AB_2904565 ), COL3A1 (liver; 1:1000; Proteintech Cat# 22734-1-AP, RRID: AB_2879158 ) or AHR (colon; 1:200; Novus Cat# NB100-2289, RRID: AB_10002581 ) for 60 min, followed by poly-HRP IgG secondary antibody.

    Techniques: Immunohistochemistry, Liquid Chromatography with Mass Spectroscopy, Gene Expression