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serum tnf α levels  (Elabscience Biotechnology)


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    Elabscience Biotechnology serum tnf α levels
    DDR2 overexpression in hepatocytes mitigates gluconeogenesis and lipid deposition in db/db mice. ( A ) Pattern diagram of treated mice ( n = 6). ( B–C ) DDR2 mRNA ( B ) and protein ( C ) levels in the livers of db/db mice, 11 days following infection with Ad-GFP or Ad-DDR2 ( n = 6). ( D ) Representative electron microscopy images of liver sections, scale bar 1 μm; H&E-stained sections, scale bar 50 μm; Oil Red O-stained sections, scale bar 50 μm and F4/80 staining, scale bar 30 μm. ( E ) Serum glucose concentrations in 6-hour-fasted db/db mice. ( F ) Reduced serum TG induced by DDR2 overexpression. ( G ) GTT performed in Ad-GFP- or Ad-DDR2-injected db/db mice, 9 days post-injection. ( H ) PEPCK and Pgc-1α protein level in liver tissues from the two groups. ( I ) There was no significant change in TG content in the liver. ( J ) AMPK and ACC phosphorylation and Srebp-1c, Fasn and Scd-1 protein levels in liver tissue. ( K ) Reduced <t>serum</t> <t>TNF-α</t> contents following DDR2 overexpression. ( L ) eIF-2α and IRE-1α phosphorylation in mouse livers. Data are shown as mean ± SEM, with comparisons by univariate t-tests. * P < 0.05, ** P < 0.01, *** P < 0.001.
    Serum Tnf α Levels, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 99 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/serum+tnf+%CE%B1+levels/pmc13083835-185-0-10?v=Elabscience+Biotechnology
    Average 95 stars, based on 99 article reviews
    serum tnf α levels - by Bioz Stars, 2026-08
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    1) Product Images from "DDR2 ameliorates nonalcoholic hepatic steatosis by activating the AMPK/ACC pathway"

    Article Title: DDR2 ameliorates nonalcoholic hepatic steatosis by activating the AMPK/ACC pathway

    Journal: Scientific Reports

    doi: 10.1038/s41598-026-42992-0

    DDR2 overexpression in hepatocytes mitigates gluconeogenesis and lipid deposition in db/db mice. ( A ) Pattern diagram of treated mice ( n = 6). ( B–C ) DDR2 mRNA ( B ) and protein ( C ) levels in the livers of db/db mice, 11 days following infection with Ad-GFP or Ad-DDR2 ( n = 6). ( D ) Representative electron microscopy images of liver sections, scale bar 1 μm; H&E-stained sections, scale bar 50 μm; Oil Red O-stained sections, scale bar 50 μm and F4/80 staining, scale bar 30 μm. ( E ) Serum glucose concentrations in 6-hour-fasted db/db mice. ( F ) Reduced serum TG induced by DDR2 overexpression. ( G ) GTT performed in Ad-GFP- or Ad-DDR2-injected db/db mice, 9 days post-injection. ( H ) PEPCK and Pgc-1α protein level in liver tissues from the two groups. ( I ) There was no significant change in TG content in the liver. ( J ) AMPK and ACC phosphorylation and Srebp-1c, Fasn and Scd-1 protein levels in liver tissue. ( K ) Reduced serum TNF-α contents following DDR2 overexpression. ( L ) eIF-2α and IRE-1α phosphorylation in mouse livers. Data are shown as mean ± SEM, with comparisons by univariate t-tests. * P < 0.05, ** P < 0.01, *** P < 0.001.
    Figure Legend Snippet: DDR2 overexpression in hepatocytes mitigates gluconeogenesis and lipid deposition in db/db mice. ( A ) Pattern diagram of treated mice ( n = 6). ( B–C ) DDR2 mRNA ( B ) and protein ( C ) levels in the livers of db/db mice, 11 days following infection with Ad-GFP or Ad-DDR2 ( n = 6). ( D ) Representative electron microscopy images of liver sections, scale bar 1 μm; H&E-stained sections, scale bar 50 μm; Oil Red O-stained sections, scale bar 50 μm and F4/80 staining, scale bar 30 μm. ( E ) Serum glucose concentrations in 6-hour-fasted db/db mice. ( F ) Reduced serum TG induced by DDR2 overexpression. ( G ) GTT performed in Ad-GFP- or Ad-DDR2-injected db/db mice, 9 days post-injection. ( H ) PEPCK and Pgc-1α protein level in liver tissues from the two groups. ( I ) There was no significant change in TG content in the liver. ( J ) AMPK and ACC phosphorylation and Srebp-1c, Fasn and Scd-1 protein levels in liver tissue. ( K ) Reduced serum TNF-α contents following DDR2 overexpression. ( L ) eIF-2α and IRE-1α phosphorylation in mouse livers. Data are shown as mean ± SEM, with comparisons by univariate t-tests. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Techniques Used: Over Expression, Infection, Electron Microscopy, Staining, Injection, Phospho-proteomics



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    DDR2 overexpression in hepatocytes mitigates gluconeogenesis and lipid deposition in db/db mice. ( A ) Pattern diagram of treated mice ( n = 6). ( B–C ) DDR2 mRNA ( B ) and protein ( C ) levels in the livers of db/db mice, 11 days following infection with Ad-GFP or Ad-DDR2 ( n = 6). ( D ) Representative electron microscopy images of liver sections, scale bar 1 μm; H&E-stained sections, scale bar 50 μm; Oil Red O-stained sections, scale bar 50 μm and F4/80 staining, scale bar 30 μm. ( E ) Serum glucose concentrations in 6-hour-fasted db/db mice. ( F ) Reduced serum TG induced by DDR2 overexpression. ( G ) GTT performed in Ad-GFP- or Ad-DDR2-injected db/db mice, 9 days post-injection. ( H ) PEPCK and Pgc-1α protein level in liver tissues from the two groups. ( I ) There was no significant change in TG content in the liver. ( J ) AMPK and ACC phosphorylation and Srebp-1c, Fasn and Scd-1 protein levels in liver tissue. ( K ) Reduced <t>serum</t> <t>TNF-α</t> contents following DDR2 overexpression. ( L ) eIF-2α and IRE-1α phosphorylation in mouse livers. Data are shown as mean ± SEM, with comparisons by univariate t-tests. * P < 0.05, ** P < 0.01, *** P < 0.001.
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    DDR2 overexpression in hepatocytes mitigates gluconeogenesis and lipid deposition in db/db mice. ( A ) Pattern diagram of treated mice ( n = 6). ( B–C ) DDR2 mRNA ( B ) and protein ( C ) levels in the livers of db/db mice, 11 days following infection with Ad-GFP or Ad-DDR2 ( n = 6). ( D ) Representative electron microscopy images of liver sections, scale bar 1 μm; H&E-stained sections, scale bar 50 μm; Oil Red O-stained sections, scale bar 50 μm and F4/80 staining, scale bar 30 μm. ( E ) Serum glucose concentrations in 6-hour-fasted db/db mice. ( F ) Reduced serum TG induced by DDR2 overexpression. ( G ) GTT performed in Ad-GFP- or Ad-DDR2-injected db/db mice, 9 days post-injection. ( H ) PEPCK and Pgc-1α protein level in liver tissues from the two groups. ( I ) There was no significant change in TG content in the liver. ( J ) AMPK and ACC phosphorylation and Srebp-1c, Fasn and Scd-1 protein levels in liver tissue. ( K ) Reduced serum TNF-α contents following DDR2 overexpression. ( L ) eIF-2α and IRE-1α phosphorylation in mouse livers. Data are shown as mean ± SEM, with comparisons by univariate t-tests. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Scientific Reports

    Article Title: DDR2 ameliorates nonalcoholic hepatic steatosis by activating the AMPK/ACC pathway

    doi: 10.1038/s41598-026-42992-0

    Figure Lengend Snippet: DDR2 overexpression in hepatocytes mitigates gluconeogenesis and lipid deposition in db/db mice. ( A ) Pattern diagram of treated mice ( n = 6). ( B–C ) DDR2 mRNA ( B ) and protein ( C ) levels in the livers of db/db mice, 11 days following infection with Ad-GFP or Ad-DDR2 ( n = 6). ( D ) Representative electron microscopy images of liver sections, scale bar 1 μm; H&E-stained sections, scale bar 50 μm; Oil Red O-stained sections, scale bar 50 μm and F4/80 staining, scale bar 30 μm. ( E ) Serum glucose concentrations in 6-hour-fasted db/db mice. ( F ) Reduced serum TG induced by DDR2 overexpression. ( G ) GTT performed in Ad-GFP- or Ad-DDR2-injected db/db mice, 9 days post-injection. ( H ) PEPCK and Pgc-1α protein level in liver tissues from the two groups. ( I ) There was no significant change in TG content in the liver. ( J ) AMPK and ACC phosphorylation and Srebp-1c, Fasn and Scd-1 protein levels in liver tissue. ( K ) Reduced serum TNF-α contents following DDR2 overexpression. ( L ) eIF-2α and IRE-1α phosphorylation in mouse livers. Data are shown as mean ± SEM, with comparisons by univariate t-tests. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: Serum TNF-α levels were ascertained through an ELISA kit (E-MSEL-M0002, Elabscience Biotechnology Inc., Wuhan, China).

    Techniques: Over Expression, Infection, Electron Microscopy, Staining, Injection, Phospho-proteomics