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multi-analyte inflammatory cytokine elisarray kit  (Qiagen)


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    Qiagen multi-analyte inflammatory cytokine elisarray kit
    The effect of carbon black (CB), urban dust (UD), and nanoparticulate carbon black (NPCB) on cell membrane damage (( A ); lactate dehydrogenase (LDH) release), oxidative stress ( B ), DNA damage ( C ), and phagocytosis ( D ) in human monocytes (M), and monocyte-derived macrophages (MDM). The inflammatory response (TNFα; ( E )) to lipopolysaccharide (100 ng/mL for 24 h) is also included ( F ). All PMs were used at 100 µg/mL and the incubation time was 24 h. Cell transition was induced by phorbol-12-myristate 13-acetate (PMA; 100 nM) applied for 72 h. LDH was measured with CyQUANT LDH Cytotoxicity Assay kit, DNA ploidy was quantified using propidium iodide staining, intracellular oxidative stress was measured using 5-(and-6)-Carboxy-2′,7′-dichlorodihydrofluorescein diacetate (carboxy-H2DCFDA) while phagocytosis was assessed with fluorescent beads (Cayman Phagocytosis kit). Fluorescence was quantified with flow cytometry. TNFα was measured in the culture medium using a Multi-Analyte Inflammatory <t>Cytokine</t> <t>ELISArray</t> Kit (Quiagen, Wroclaw, Poland). Data are means ± SD of 6–10 assays. * p < 0.05; ** p < 0.01 for comparisons with the corresponding control cells; ^^ p < 0.01 for comparisons with corresponding naive cells; # p < 0.05 for comparisons with LPS-treated cells.
    Multi Analyte Inflammatory Cytokine Elisarray Kit, supplied by Qiagen, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/multi-analyte+elisarray+kit/pmc11352816-86-13-18?v=Qiagen
    Average 90 stars, based on 1 article reviews
    multi-analyte inflammatory cytokine elisarray kit - by Bioz Stars, 2026-08
    90/100 stars

    Images

    1) Product Images from "Signalling Pathways of Inflammation and Cancer in Human Mononuclear Cells: Effect of Nanoparticle Air Pollutants"

    Article Title: Signalling Pathways of Inflammation and Cancer in Human Mononuclear Cells: Effect of Nanoparticle Air Pollutants

    Journal: Cells

    doi: 10.3390/cells13161367

    The effect of carbon black (CB), urban dust (UD), and nanoparticulate carbon black (NPCB) on cell membrane damage (( A ); lactate dehydrogenase (LDH) release), oxidative stress ( B ), DNA damage ( C ), and phagocytosis ( D ) in human monocytes (M), and monocyte-derived macrophages (MDM). The inflammatory response (TNFα; ( E )) to lipopolysaccharide (100 ng/mL for 24 h) is also included ( F ). All PMs were used at 100 µg/mL and the incubation time was 24 h. Cell transition was induced by phorbol-12-myristate 13-acetate (PMA; 100 nM) applied for 72 h. LDH was measured with CyQUANT LDH Cytotoxicity Assay kit, DNA ploidy was quantified using propidium iodide staining, intracellular oxidative stress was measured using 5-(and-6)-Carboxy-2′,7′-dichlorodihydrofluorescein diacetate (carboxy-H2DCFDA) while phagocytosis was assessed with fluorescent beads (Cayman Phagocytosis kit). Fluorescence was quantified with flow cytometry. TNFα was measured in the culture medium using a Multi-Analyte Inflammatory Cytokine ELISArray Kit (Quiagen, Wroclaw, Poland). Data are means ± SD of 6–10 assays. * p < 0.05; ** p < 0.01 for comparisons with the corresponding control cells; ^^ p < 0.01 for comparisons with corresponding naive cells; # p < 0.05 for comparisons with LPS-treated cells.
    Figure Legend Snippet: The effect of carbon black (CB), urban dust (UD), and nanoparticulate carbon black (NPCB) on cell membrane damage (( A ); lactate dehydrogenase (LDH) release), oxidative stress ( B ), DNA damage ( C ), and phagocytosis ( D ) in human monocytes (M), and monocyte-derived macrophages (MDM). The inflammatory response (TNFα; ( E )) to lipopolysaccharide (100 ng/mL for 24 h) is also included ( F ). All PMs were used at 100 µg/mL and the incubation time was 24 h. Cell transition was induced by phorbol-12-myristate 13-acetate (PMA; 100 nM) applied for 72 h. LDH was measured with CyQUANT LDH Cytotoxicity Assay kit, DNA ploidy was quantified using propidium iodide staining, intracellular oxidative stress was measured using 5-(and-6)-Carboxy-2′,7′-dichlorodihydrofluorescein diacetate (carboxy-H2DCFDA) while phagocytosis was assessed with fluorescent beads (Cayman Phagocytosis kit). Fluorescence was quantified with flow cytometry. TNFα was measured in the culture medium using a Multi-Analyte Inflammatory Cytokine ELISArray Kit (Quiagen, Wroclaw, Poland). Data are means ± SD of 6–10 assays. * p < 0.05; ** p < 0.01 for comparisons with the corresponding control cells; ^^ p < 0.01 for comparisons with corresponding naive cells; # p < 0.05 for comparisons with LPS-treated cells.

    Techniques Used: Membrane, Derivative Assay, Incubation, CyQUANT Assay, LDH Cytotoxicity Assay, Staining, Fluorescence, Flow Cytometry, Control



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    The effect of carbon black (CB), urban dust (UD), and nanoparticulate carbon black (NPCB) on cell membrane damage (( A ); lactate dehydrogenase (LDH) release), oxidative stress ( B ), DNA damage ( C ), and phagocytosis ( D ) in human monocytes (M), and monocyte-derived macrophages (MDM). The inflammatory response (TNFα; ( E )) to lipopolysaccharide (100 ng/mL for 24 h) is also included ( F ). All PMs were used at 100 µg/mL and the incubation time was 24 h. Cell transition was induced by phorbol-12-myristate 13-acetate (PMA; 100 nM) applied for 72 h. LDH was measured with CyQUANT LDH Cytotoxicity Assay kit, DNA ploidy was quantified using propidium iodide staining, intracellular oxidative stress was measured using 5-(and-6)-Carboxy-2′,7′-dichlorodihydrofluorescein diacetate (carboxy-H2DCFDA) while phagocytosis was assessed with fluorescent beads (Cayman Phagocytosis kit). Fluorescence was quantified with flow cytometry. TNFα was measured in the culture medium using a Multi-Analyte Inflammatory <t>Cytokine</t> <t>ELISArray</t> Kit (Quiagen, Wroclaw, Poland). Data are means ± SD of 6–10 assays. * p < 0.05; ** p < 0.01 for comparisons with the corresponding control cells; ^^ p < 0.01 for comparisons with corresponding naive cells; # p < 0.05 for comparisons with LPS-treated cells.
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    The effect of carbon black (CB), urban dust (UD), and nanoparticulate carbon black (NPCB) on cell membrane damage (( A ); lactate dehydrogenase (LDH) release), oxidative stress ( B ), DNA damage ( C ), and phagocytosis ( D ) in human monocytes (M), and monocyte-derived macrophages (MDM). The inflammatory response (TNFα; ( E )) to lipopolysaccharide (100 ng/mL for 24 h) is also included ( F ). All PMs were used at 100 µg/mL and the incubation time was 24 h. Cell transition was induced by phorbol-12-myristate 13-acetate (PMA; 100 nM) applied for 72 h. LDH was measured with CyQUANT LDH Cytotoxicity Assay kit, DNA ploidy was quantified using propidium iodide staining, intracellular oxidative stress was measured using 5-(and-6)-Carboxy-2′,7′-dichlorodihydrofluorescein diacetate (carboxy-H2DCFDA) while phagocytosis was assessed with fluorescent beads (Cayman Phagocytosis kit). Fluorescence was quantified with flow cytometry. TNFα was measured in the culture medium using a Multi-Analyte Inflammatory Cytokine ELISArray Kit (Quiagen, Wroclaw, Poland). Data are means ± SD of 6–10 assays. * p < 0.05; ** p < 0.01 for comparisons with the corresponding control cells; ^^ p < 0.01 for comparisons with corresponding naive cells; # p < 0.05 for comparisons with LPS-treated cells.

    Journal: Cells

    Article Title: Signalling Pathways of Inflammation and Cancer in Human Mononuclear Cells: Effect of Nanoparticle Air Pollutants

    doi: 10.3390/cells13161367

    Figure Lengend Snippet: The effect of carbon black (CB), urban dust (UD), and nanoparticulate carbon black (NPCB) on cell membrane damage (( A ); lactate dehydrogenase (LDH) release), oxidative stress ( B ), DNA damage ( C ), and phagocytosis ( D ) in human monocytes (M), and monocyte-derived macrophages (MDM). The inflammatory response (TNFα; ( E )) to lipopolysaccharide (100 ng/mL for 24 h) is also included ( F ). All PMs were used at 100 µg/mL and the incubation time was 24 h. Cell transition was induced by phorbol-12-myristate 13-acetate (PMA; 100 nM) applied for 72 h. LDH was measured with CyQUANT LDH Cytotoxicity Assay kit, DNA ploidy was quantified using propidium iodide staining, intracellular oxidative stress was measured using 5-(and-6)-Carboxy-2′,7′-dichlorodihydrofluorescein diacetate (carboxy-H2DCFDA) while phagocytosis was assessed with fluorescent beads (Cayman Phagocytosis kit). Fluorescence was quantified with flow cytometry. TNFα was measured in the culture medium using a Multi-Analyte Inflammatory Cytokine ELISArray Kit (Quiagen, Wroclaw, Poland). Data are means ± SD of 6–10 assays. * p < 0.05; ** p < 0.01 for comparisons with the corresponding control cells; ^^ p < 0.01 for comparisons with corresponding naive cells; # p < 0.05 for comparisons with LPS-treated cells.

    Article Snippet: TNFα was quantified in the culture medium of M and MDM with the Multi-Analyte Inflammatory Cytokine ELISArray Kit (Qiagen, Manchester, UK).

    Techniques: Membrane, Derivative Assay, Incubation, CyQUANT Assay, LDH Cytotoxicity Assay, Staining, Fluorescence, Flow Cytometry, Control