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interleukin 1 receptor antagonist jo urn al p e p roo f  (MedChemExpress)


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    MedChemExpress interleukin 1 receptor antagonist jo urn al p e p roo f
    Interleukin 1 Receptor Antagonist Jo Urn Al P E P Roo F, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    MedChemExpress interleukin 1 receptor antagonist jo urn al p e p roo f
    Interleukin 1 Receptor Antagonist Jo Urn Al P E P Roo F, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    GCDCA-mediated hepatocyte IL-1β secretion activates HSCs. ( A ) Western blot analysis ofα-SMA and Collagen-I in LX2 cells treated with conditioned medium (CM) from GCDCA/LPS-stimulated L02 hepatocytes. ( B ) The protein levels of α-SMA and Collagen-I in LX2 cells with treatment of IL-1 receptor antagonist <t>(IL-1RA,</t> 200 ng/mL) upon CM exposure. ( C and D ) Representative images and quantification of LX2 migration upon CM exposure detected by wound healing assay. ( E ) CCK-8 assay of LX2 proliferation by CM treatment. n ≥ 3 for each group. a P < 0.05.
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    GCDCA-mediated hepatocyte IL-1β secretion activates HSCs. ( A ) Western blot analysis ofα-SMA and Collagen-I in LX2 cells treated with conditioned medium (CM) from GCDCA/LPS-stimulated L02 hepatocytes. ( B ) The protein levels of α-SMA and Collagen-I in LX2 cells with treatment of IL-1 receptor antagonist <t>(IL-1RA,</t> 200 ng/mL) upon CM exposure. ( C and D ) Representative images and quantification of LX2 migration upon CM exposure detected by wound healing assay. ( E ) CCK-8 assay of LX2 proliferation by CM treatment. n ≥ 3 for each group. a P < 0.05.
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    GCDCA-mediated hepatocyte IL-1β secretion activates HSCs. ( A ) Western blot analysis ofα-SMA and Collagen-I in LX2 cells treated with conditioned medium (CM) from GCDCA/LPS-stimulated L02 hepatocytes. ( B ) The protein levels of α-SMA and Collagen-I in LX2 cells with treatment of IL-1 receptor antagonist <t>(IL-1RA,</t> 200 ng/mL) upon CM exposure. ( C and D ) Representative images and quantification of LX2 migration upon CM exposure detected by wound healing assay. ( E ) CCK-8 assay of LX2 proliferation by CM treatment. n ≥ 3 for each group. a P < 0.05.
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    Blocking IL-1β in the RA serum attenuates glycolysis-HIF-1α axis mediated IL-1β. (A) qPCR analysis of HK2, HIF-1α, and IL-1β mRNA expression in HMDMs stimulated for 24 h with IL-1β, TNF-α, GM-CSF, IFN-γ, or IL-6 ( n = 7).( B )Representative image of IL-1β and HIF-1α expression in HMDMs pretreated with or without 2-DG (5 mM, 3 h) followed by 24 h stimulation with IL-1β, TNF-α, or GM-CSF ( n = 4).( C )Extracellular acidification rate (ECAR) measured by Seahorse assay in HMDMs exposed to RA serum with or without <t>IL-1RN,</t> infliximab, or lenzilumab ( n = 6).( D-E ) Western blot analysis of HIF-1α and IL-1β expression in macrophages treated with RA serum in the presence or absence of ( D ) IL-1RN or ( E ) infliximab for 24 h ( n = 6).Data were shown as mean ± SEM and were analyzed using one-way ANOVA or Two-tailed student’s t-test. *, p < 0.05; **, p < 0.01. 2-DG: 2-Deoxy-D-glucose; <t>IL-1RN:</t> <t>Interleukin-1</t> receptor antagonist; IFX: Infliximab
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    Blocking IL-1β in the RA serum attenuates glycolysis-HIF-1α axis mediated IL-1β. (A) qPCR analysis of HK2, HIF-1α, and IL-1β mRNA expression in HMDMs stimulated for 24 h with IL-1β, TNF-α, GM-CSF, IFN-γ, or IL-6 ( n = 7).( B )Representative image of IL-1β and HIF-1α expression in HMDMs pretreated with or without 2-DG (5 mM, 3 h) followed by 24 h stimulation with IL-1β, TNF-α, or GM-CSF ( n = 4).( C )Extracellular acidification rate (ECAR) measured by Seahorse assay in HMDMs exposed to RA serum with or without <t>IL-1RN,</t> infliximab, or lenzilumab ( n = 6).( D-E ) Western blot analysis of HIF-1α and IL-1β expression in macrophages treated with RA serum in the presence or absence of ( D ) IL-1RN or ( E ) infliximab for 24 h ( n = 6).Data were shown as mean ± SEM and were analyzed using one-way ANOVA or Two-tailed student’s t-test. *, p < 0.05; **, p < 0.01. 2-DG: 2-Deoxy-D-glucose; <t>IL-1RN:</t> <t>Interleukin-1</t> receptor antagonist; IFX: Infliximab
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    Blocking IL-1β in the RA serum attenuates glycolysis-HIF-1α axis mediated IL-1β. (A) qPCR analysis of HK2, HIF-1α, and IL-1β mRNA expression in HMDMs stimulated for 24 h with IL-1β, TNF-α, GM-CSF, IFN-γ, or IL-6 ( n = 7).( B )Representative image of IL-1β and HIF-1α expression in HMDMs pretreated with or without 2-DG (5 mM, 3 h) followed by 24 h stimulation with IL-1β, TNF-α, or GM-CSF ( n = 4).( C )Extracellular acidification rate (ECAR) measured by Seahorse assay in HMDMs exposed to RA serum with or without <t>IL-1RN,</t> infliximab, or lenzilumab ( n = 6).( D-E ) Western blot analysis of HIF-1α and IL-1β expression in macrophages treated with RA serum in the presence or absence of ( D ) IL-1RN or ( E ) infliximab for 24 h ( n = 6).Data were shown as mean ± SEM and were analyzed using one-way ANOVA or Two-tailed student’s t-test. *, p < 0.05; **, p < 0.01. 2-DG: 2-Deoxy-D-glucose; <t>IL-1RN:</t> <t>Interleukin-1</t> receptor antagonist; IFX: Infliximab
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    Blocking IL-1β in the RA serum attenuates glycolysis-HIF-1α axis mediated IL-1β. (A) qPCR analysis of HK2, HIF-1α, and IL-1β mRNA expression in HMDMs stimulated for 24 h with IL-1β, TNF-α, GM-CSF, IFN-γ, or IL-6 ( n = 7).( B )Representative image of IL-1β and HIF-1α expression in HMDMs pretreated with or without 2-DG (5 mM, 3 h) followed by 24 h stimulation with IL-1β, TNF-α, or GM-CSF ( n = 4).( C )Extracellular acidification rate (ECAR) measured by Seahorse assay in HMDMs exposed to RA serum with or without <t>IL-1RN,</t> infliximab, or lenzilumab ( n = 6).( D-E ) Western blot analysis of HIF-1α and IL-1β expression in macrophages treated with RA serum in the presence or absence of ( D ) IL-1RN or ( E ) infliximab for 24 h ( n = 6).Data were shown as mean ± SEM and were analyzed using one-way ANOVA or Two-tailed student’s t-test. *, p < 0.05; **, p < 0.01. 2-DG: 2-Deoxy-D-glucose; <t>IL-1RN:</t> <t>Interleukin-1</t> receptor antagonist; IFX: Infliximab
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    Image Search Results


    GCDCA-mediated hepatocyte IL-1β secretion activates HSCs. ( A ) Western blot analysis ofα-SMA and Collagen-I in LX2 cells treated with conditioned medium (CM) from GCDCA/LPS-stimulated L02 hepatocytes. ( B ) The protein levels of α-SMA and Collagen-I in LX2 cells with treatment of IL-1 receptor antagonist (IL-1RA, 200 ng/mL) upon CM exposure. ( C and D ) Representative images and quantification of LX2 migration upon CM exposure detected by wound healing assay. ( E ) CCK-8 assay of LX2 proliferation by CM treatment. n ≥ 3 for each group. a P < 0.05.

    Journal: Journal of Inflammation Research

    Article Title: Glycochenodeoxycholic acid induces the release of IL-1beta from L02 cells via the NLRP3/caspase-1/GSDMD pathway to activate LX2 cells

    doi: 10.2147/JIR.S532042

    Figure Lengend Snippet: GCDCA-mediated hepatocyte IL-1β secretion activates HSCs. ( A ) Western blot analysis ofα-SMA and Collagen-I in LX2 cells treated with conditioned medium (CM) from GCDCA/LPS-stimulated L02 hepatocytes. ( B ) The protein levels of α-SMA and Collagen-I in LX2 cells with treatment of IL-1 receptor antagonist (IL-1RA, 200 ng/mL) upon CM exposure. ( C and D ) Representative images and quantification of LX2 migration upon CM exposure detected by wound healing assay. ( E ) CCK-8 assay of LX2 proliferation by CM treatment. n ≥ 3 for each group. a P < 0.05.

    Article Snippet: Conditioned media from treated L02 cells were co-cultured with LX2 cells in the presence/absence of Interleukin-1 receptor antagonist (IL-1RA) (200 ng/mL, HY-P7029A, MCE).

    Techniques: Western Blot, Migration, Wound Healing Assay, CCK-8 Assay

    Blocking IL-1β in the RA serum attenuates glycolysis-HIF-1α axis mediated IL-1β. (A) qPCR analysis of HK2, HIF-1α, and IL-1β mRNA expression in HMDMs stimulated for 24 h with IL-1β, TNF-α, GM-CSF, IFN-γ, or IL-6 ( n = 7).( B )Representative image of IL-1β and HIF-1α expression in HMDMs pretreated with or without 2-DG (5 mM, 3 h) followed by 24 h stimulation with IL-1β, TNF-α, or GM-CSF ( n = 4).( C )Extracellular acidification rate (ECAR) measured by Seahorse assay in HMDMs exposed to RA serum with or without IL-1RN, infliximab, or lenzilumab ( n = 6).( D-E ) Western blot analysis of HIF-1α and IL-1β expression in macrophages treated with RA serum in the presence or absence of ( D ) IL-1RN or ( E ) infliximab for 24 h ( n = 6).Data were shown as mean ± SEM and were analyzed using one-way ANOVA or Two-tailed student’s t-test. *, p < 0.05; **, p < 0.01. 2-DG: 2-Deoxy-D-glucose; IL-1RN: Interleukin-1 receptor antagonist; IFX: Infliximab

    Journal: Arthritis Research & Therapy

    Article Title: The Glycolysis-HIF-1α axis induces IL-1β of macrophages in rheumatoid arthritis

    doi: 10.1186/s13075-025-03647-z

    Figure Lengend Snippet: Blocking IL-1β in the RA serum attenuates glycolysis-HIF-1α axis mediated IL-1β. (A) qPCR analysis of HK2, HIF-1α, and IL-1β mRNA expression in HMDMs stimulated for 24 h with IL-1β, TNF-α, GM-CSF, IFN-γ, or IL-6 ( n = 7).( B )Representative image of IL-1β and HIF-1α expression in HMDMs pretreated with or without 2-DG (5 mM, 3 h) followed by 24 h stimulation with IL-1β, TNF-α, or GM-CSF ( n = 4).( C )Extracellular acidification rate (ECAR) measured by Seahorse assay in HMDMs exposed to RA serum with or without IL-1RN, infliximab, or lenzilumab ( n = 6).( D-E ) Western blot analysis of HIF-1α and IL-1β expression in macrophages treated with RA serum in the presence or absence of ( D ) IL-1RN or ( E ) infliximab for 24 h ( n = 6).Data were shown as mean ± SEM and were analyzed using one-way ANOVA or Two-tailed student’s t-test. *, p < 0.05; **, p < 0.01. 2-DG: 2-Deoxy-D-glucose; IL-1RN: Interleukin-1 receptor antagonist; IFX: Infliximab

    Article Snippet: For cytokine blocking, HMDMs were incubated with RA serum with 100ng/ml of Interleukin-1 receptor antagonist (IL-1RN, HY-P7029, MedChemExpress), 10 μg/ml of Infliximab (HY-P9970, MedChemExpress), or Lenzilumab (HY-P99207, MedChemExpress) for 24 h, respectively.

    Techniques: Blocking Assay, Expressing, Western Blot, Two Tailed Test