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il 18 elisa kit  (Elabscience Biotechnology)


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    Structured Review

    Elabscience Biotechnology il 18 elisa kit
    Il 18 Elisa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 97/100, based on 435 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 97 stars, based on 435 article reviews
    il 18 elisa kit - by Bioz Stars, 2026-04
    97/100 stars

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    (A) qPCR analysis of NLRP3 mRNA in BV2 cells treated with vehicle (PBS), LPS/ATP, or LPS/ATP + MCC950. Data are expressed as mean ± SD of 3 biologically independent experiments. (B) Representative Western blots and quantification of NLRP3, pro-caspase-1, and cleaved caspase-1 (p20) protein levels. β-actin served as a loading control. Data are expressed as mean ± SD of 3 biologically independent experiments. (C) Caspase-1 activity measured using a commercial assay kit. Data are expressed as mean ± SD of 3 biologically independent experiments. (D and E) Secretion levels of mature IL-1β <t>and</t> <t>IL-18</t> in cell culture supernatants determined by ELISA. Data are expressed as mean ± SD of 3 biologically independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, n.s. non-significant.
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    (A) qPCR analysis of NLRP3 mRNA in BV2 cells treated with vehicle (PBS), LPS/ATP, or LPS/ATP + MCC950. Data are expressed as mean ± SD of 3 biologically independent experiments. (B) Representative Western blots and quantification of NLRP3, pro-caspase-1, and cleaved caspase-1 (p20) protein levels. β-actin served as a loading control. Data are expressed as mean ± SD of 3 biologically independent experiments. (C) Caspase-1 activity measured using a commercial assay kit. Data are expressed as mean ± SD of 3 biologically independent experiments. (D and E) Secretion levels of mature IL-1β <t>and</t> <t>IL-18</t> in cell culture supernatants determined by ELISA. Data are expressed as mean ± SD of 3 biologically independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, n.s. non-significant.
    Il 18 Elisa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    (A) qPCR analysis of NLRP3 mRNA in BV2 cells treated with vehicle (PBS), LPS/ATP, or LPS/ATP + MCC950. Data are expressed as mean ± SD of 3 biologically independent experiments. (B) Representative Western blots and quantification of NLRP3, pro-caspase-1, and cleaved caspase-1 (p20) protein levels. β-actin served as a loading control. Data are expressed as mean ± SD of 3 biologically independent experiments. (C) Caspase-1 activity measured using a commercial assay kit. Data are expressed as mean ± SD of 3 biologically independent experiments. (D and E) Secretion levels of mature IL-1β <t>and</t> <t>IL-18</t> in cell culture supernatants determined by ELISA. Data are expressed as mean ± SD of 3 biologically independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, n.s. non-significant.
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    (A) qPCR analysis of NLRP3 mRNA in BV2 cells treated with vehicle (PBS), LPS/ATP, or LPS/ATP + MCC950. Data are expressed as mean ± SD of 3 biologically independent experiments. (B) Representative Western blots and quantification of NLRP3, pro-caspase-1, and cleaved caspase-1 (p20) protein levels. β-actin served as a loading control. Data are expressed as mean ± SD of 3 biologically independent experiments. (C) Caspase-1 activity measured using a commercial assay kit. Data are expressed as mean ± SD of 3 biologically independent experiments. (D and E) Secretion levels of mature IL-1β <t>and</t> <t>IL-18</t> in cell culture supernatants determined by ELISA. Data are expressed as mean ± SD of 3 biologically independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, n.s. non-significant.
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    (A) qPCR analysis of NLRP3 mRNA in BV2 cells treated with vehicle (PBS), LPS/ATP, or LPS/ATP + MCC950. Data are expressed as mean ± SD of 3 biologically independent experiments. (B) Representative Western blots and quantification of NLRP3, pro-caspase-1, and cleaved caspase-1 (p20) protein levels. β-actin served as a loading control. Data are expressed as mean ± SD of 3 biologically independent experiments. (C) Caspase-1 activity measured using a commercial assay kit. Data are expressed as mean ± SD of 3 biologically independent experiments. (D and E) Secretion levels of mature IL-1β <t>and</t> <t>IL-18</t> in cell culture supernatants determined by ELISA. Data are expressed as mean ± SD of 3 biologically independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, n.s. non-significant.
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    Inflammatory profiles of sJIA patients and neuro–inflammation co-analysis reveal correlations between HMOX2 and <t>IL-6/IL-18.</t> (A) PCA plot of inflammation-related plasma proteins showing separation between active sJIA patients and HCs. Each point represents one subject (n = 32; 16 active sJIA and 16 HCs). (B) Volcano plot of DEPs in active sJIA vs. HC. Dashed lines indicate significance thresholds. (C) Volcano plot of DEPs in Cluster 2 active sJIA vs. Cluster 1 active sJIA. Dashed lines indicate significance thresholds. (D) PCA plot of inflammation related plasma proteins showing the distribution of sJIA patients (active vs inactive) and HCs. Each point represents one subject, with lines connecting paired active and inactive samples from the same patient (n = 36; 12 active sJIA, 12 inactive sJIA, and 12 HCs). (E) Bubble plot showing correlations between DEPs from the inflammation panel and DEPs from the neuro panel in active sJIA patients. (F) Correlation analysis showing significant negative correlations between HMOX2 and IL-6/IL-18. (G-H) Line plot showing longitudinal changes of IL-6 and IL-18 from healthy to active to inactive sJIA. Statistics: (B) paired t-test with Benjamini–Hochberg correction for multiple comparisons; (C) unpaired t-test with Benjamini–Hochberg correction for multiple comparisons; (E, F) Pearson correlation analysis; (G, H) Multiple paired t-tests with Holm–Bonferroni adjustment.
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    Inflammatory profiles of sJIA patients and neuro–inflammation co-analysis reveal correlations between HMOX2 and <t>IL-6/IL-18.</t> (A) PCA plot of inflammation-related plasma proteins showing separation between active sJIA patients and HCs. Each point represents one subject (n = 32; 16 active sJIA and 16 HCs). (B) Volcano plot of DEPs in active sJIA vs. HC. Dashed lines indicate significance thresholds. (C) Volcano plot of DEPs in Cluster 2 active sJIA vs. Cluster 1 active sJIA. Dashed lines indicate significance thresholds. (D) PCA plot of inflammation related plasma proteins showing the distribution of sJIA patients (active vs inactive) and HCs. Each point represents one subject, with lines connecting paired active and inactive samples from the same patient (n = 36; 12 active sJIA, 12 inactive sJIA, and 12 HCs). (E) Bubble plot showing correlations between DEPs from the inflammation panel and DEPs from the neuro panel in active sJIA patients. (F) Correlation analysis showing significant negative correlations between HMOX2 and IL-6/IL-18. (G-H) Line plot showing longitudinal changes of IL-6 and IL-18 from healthy to active to inactive sJIA. Statistics: (B) paired t-test with Benjamini–Hochberg correction for multiple comparisons; (C) unpaired t-test with Benjamini–Hochberg correction for multiple comparisons; (E, F) Pearson correlation analysis; (G, H) Multiple paired t-tests with Holm–Bonferroni adjustment.
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    Inflammatory profiles of sJIA patients and neuro–inflammation co-analysis reveal correlations between HMOX2 and <t>IL-6/IL-18.</t> (A) PCA plot of inflammation-related plasma proteins showing separation between active sJIA patients and HCs. Each point represents one subject (n = 32; 16 active sJIA and 16 HCs). (B) Volcano plot of DEPs in active sJIA vs. HC. Dashed lines indicate significance thresholds. (C) Volcano plot of DEPs in Cluster 2 active sJIA vs. Cluster 1 active sJIA. Dashed lines indicate significance thresholds. (D) PCA plot of inflammation related plasma proteins showing the distribution of sJIA patients (active vs inactive) and HCs. Each point represents one subject, with lines connecting paired active and inactive samples from the same patient (n = 36; 12 active sJIA, 12 inactive sJIA, and 12 HCs). (E) Bubble plot showing correlations between DEPs from the inflammation panel and DEPs from the neuro panel in active sJIA patients. (F) Correlation analysis showing significant negative correlations between HMOX2 and IL-6/IL-18. (G-H) Line plot showing longitudinal changes of IL-6 and IL-18 from healthy to active to inactive sJIA. Statistics: (B) paired t-test with Benjamini–Hochberg correction for multiple comparisons; (C) unpaired t-test with Benjamini–Hochberg correction for multiple comparisons; (E, F) Pearson correlation analysis; (G, H) Multiple paired t-tests with Holm–Bonferroni adjustment.
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    Image Search Results


    (A) qPCR analysis of NLRP3 mRNA in BV2 cells treated with vehicle (PBS), LPS/ATP, or LPS/ATP + MCC950. Data are expressed as mean ± SD of 3 biologically independent experiments. (B) Representative Western blots and quantification of NLRP3, pro-caspase-1, and cleaved caspase-1 (p20) protein levels. β-actin served as a loading control. Data are expressed as mean ± SD of 3 biologically independent experiments. (C) Caspase-1 activity measured using a commercial assay kit. Data are expressed as mean ± SD of 3 biologically independent experiments. (D and E) Secretion levels of mature IL-1β and IL-18 in cell culture supernatants determined by ELISA. Data are expressed as mean ± SD of 3 biologically independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, n.s. non-significant.

    Journal: PLOS One

    Article Title: A new mechanism regulating microglial NLRP3 inflammasome: FMR1 mediates NLRP3 mRNA stability

    doi: 10.1371/journal.pone.0341867

    Figure Lengend Snippet: (A) qPCR analysis of NLRP3 mRNA in BV2 cells treated with vehicle (PBS), LPS/ATP, or LPS/ATP + MCC950. Data are expressed as mean ± SD of 3 biologically independent experiments. (B) Representative Western blots and quantification of NLRP3, pro-caspase-1, and cleaved caspase-1 (p20) protein levels. β-actin served as a loading control. Data are expressed as mean ± SD of 3 biologically independent experiments. (C) Caspase-1 activity measured using a commercial assay kit. Data are expressed as mean ± SD of 3 biologically independent experiments. (D and E) Secretion levels of mature IL-1β and IL-18 in cell culture supernatants determined by ELISA. Data are expressed as mean ± SD of 3 biologically independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, n.s. non-significant.

    Article Snippet: The levels of IL-1β and IL-18 in the supernatant of treated BV2 microglia were determined using Mouse IL-1β ELISA Kit (#EK201B) and Mouse IL-18 ELISA Kit (#EK218), respectively, as described by the vendor (Multi Sciences, Hangzhou, China).

    Techniques: Western Blot, Control, Activity Assay, Cell Culture, Enzyme-linked Immunosorbent Assay

    (A) Measurement of NLRP3, pro-caspase-1 and cleaved caspase-1 levels by western blot in BV2 cells transfected with FMR1 expression construct, FMR1 expression construct+NLRP3 cDNA plasmid, or vector control before LPS/ATP exposure. Data are expressed as mean ± SD of 3 biologically independent experiments. (B) Evaluation of caspase-1 activity in BV2 cells treated as indicated using the assay kit. Data are expressed as mean ± SD of 3 biologically independent experiments. (C and D) Determination of IL-1β and IL-18 secretion levels by ELISA in the supernatant of BV2 cells treated as in A. Data are expressed as mean ± SD of 3 biologically independent experiments. (E) BV2 cells were transfected and treated as indicated, followed by LPS/ATP stimulation. The release of LDH into the culture supernatant was quantified as a marker of cell membrane integrity loss during pyroptosis. Data are expressed as mean ± SD of 3 biologically independent experiments. (F) FMR1 attenuates LPS/ATP-induced pyroptosis, as assessed by Calcein-AM/PI staining. Representative fluorescent micrographs (left) and quantification data (right). Nuclei were counterstained with DAPI (blue). Scale bar, 100 μm. Data are expressed as mean ± SD of 3 biologically independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: PLOS One

    Article Title: A new mechanism regulating microglial NLRP3 inflammasome: FMR1 mediates NLRP3 mRNA stability

    doi: 10.1371/journal.pone.0341867

    Figure Lengend Snippet: (A) Measurement of NLRP3, pro-caspase-1 and cleaved caspase-1 levels by western blot in BV2 cells transfected with FMR1 expression construct, FMR1 expression construct+NLRP3 cDNA plasmid, or vector control before LPS/ATP exposure. Data are expressed as mean ± SD of 3 biologically independent experiments. (B) Evaluation of caspase-1 activity in BV2 cells treated as indicated using the assay kit. Data are expressed as mean ± SD of 3 biologically independent experiments. (C and D) Determination of IL-1β and IL-18 secretion levels by ELISA in the supernatant of BV2 cells treated as in A. Data are expressed as mean ± SD of 3 biologically independent experiments. (E) BV2 cells were transfected and treated as indicated, followed by LPS/ATP stimulation. The release of LDH into the culture supernatant was quantified as a marker of cell membrane integrity loss during pyroptosis. Data are expressed as mean ± SD of 3 biologically independent experiments. (F) FMR1 attenuates LPS/ATP-induced pyroptosis, as assessed by Calcein-AM/PI staining. Representative fluorescent micrographs (left) and quantification data (right). Nuclei were counterstained with DAPI (blue). Scale bar, 100 μm. Data are expressed as mean ± SD of 3 biologically independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: The levels of IL-1β and IL-18 in the supernatant of treated BV2 microglia were determined using Mouse IL-1β ELISA Kit (#EK201B) and Mouse IL-18 ELISA Kit (#EK218), respectively, as described by the vendor (Multi Sciences, Hangzhou, China).

    Techniques: Western Blot, Transfection, Expressing, Construct, Plasmid Preparation, Control, Activity Assay, Enzyme-linked Immunosorbent Assay, Marker, Membrane, Staining

    Inflammatory profiles of sJIA patients and neuro–inflammation co-analysis reveal correlations between HMOX2 and IL-6/IL-18. (A) PCA plot of inflammation-related plasma proteins showing separation between active sJIA patients and HCs. Each point represents one subject (n = 32; 16 active sJIA and 16 HCs). (B) Volcano plot of DEPs in active sJIA vs. HC. Dashed lines indicate significance thresholds. (C) Volcano plot of DEPs in Cluster 2 active sJIA vs. Cluster 1 active sJIA. Dashed lines indicate significance thresholds. (D) PCA plot of inflammation related plasma proteins showing the distribution of sJIA patients (active vs inactive) and HCs. Each point represents one subject, with lines connecting paired active and inactive samples from the same patient (n = 36; 12 active sJIA, 12 inactive sJIA, and 12 HCs). (E) Bubble plot showing correlations between DEPs from the inflammation panel and DEPs from the neuro panel in active sJIA patients. (F) Correlation analysis showing significant negative correlations between HMOX2 and IL-6/IL-18. (G-H) Line plot showing longitudinal changes of IL-6 and IL-18 from healthy to active to inactive sJIA. Statistics: (B) paired t-test with Benjamini–Hochberg correction for multiple comparisons; (C) unpaired t-test with Benjamini–Hochberg correction for multiple comparisons; (E, F) Pearson correlation analysis; (G, H) Multiple paired t-tests with Holm–Bonferroni adjustment.

    Journal: bioRxiv

    Article Title: Hippocampal Neuroinflammation and Altered Peripheral Neurobiological Protein Profile in Experimental Arthritis and Systemic Juvenile Idiopathic Arthritis

    doi: 10.64898/2026.03.13.711607

    Figure Lengend Snippet: Inflammatory profiles of sJIA patients and neuro–inflammation co-analysis reveal correlations between HMOX2 and IL-6/IL-18. (A) PCA plot of inflammation-related plasma proteins showing separation between active sJIA patients and HCs. Each point represents one subject (n = 32; 16 active sJIA and 16 HCs). (B) Volcano plot of DEPs in active sJIA vs. HC. Dashed lines indicate significance thresholds. (C) Volcano plot of DEPs in Cluster 2 active sJIA vs. Cluster 1 active sJIA. Dashed lines indicate significance thresholds. (D) PCA plot of inflammation related plasma proteins showing the distribution of sJIA patients (active vs inactive) and HCs. Each point represents one subject, with lines connecting paired active and inactive samples from the same patient (n = 36; 12 active sJIA, 12 inactive sJIA, and 12 HCs). (E) Bubble plot showing correlations between DEPs from the inflammation panel and DEPs from the neuro panel in active sJIA patients. (F) Correlation analysis showing significant negative correlations between HMOX2 and IL-6/IL-18. (G-H) Line plot showing longitudinal changes of IL-6 and IL-18 from healthy to active to inactive sJIA. Statistics: (B) paired t-test with Benjamini–Hochberg correction for multiple comparisons; (C) unpaired t-test with Benjamini–Hochberg correction for multiple comparisons; (E, F) Pearson correlation analysis; (G, H) Multiple paired t-tests with Holm–Bonferroni adjustment.

    Article Snippet: Mouse serum samples were also used to measure IL-6 and IL-18 level using IL-6 and IL-18 mouse Elisa kits (R&D systems, USA).

    Techniques: Clinical Proteomics

    IL-6 and IL-18 are elevated in arthritic mice and synergistically trigger oxidative stress in microglia. (A) Box plots showing increased serum IL-6 and IL-18 levels in arthritic mice. (B) Correlation analysis showing a negative correlation between serum IL-18 and HMOX2, whereas IL-6 showed no significant correlation in arthritic mice. (C) Scatter plots showing the correlations between serum IL-18/IL-6 and microglial activation in arthritic mice. (D–E) Representative images of DCFH-DA staining showing ROS levels in SimA9 cells treated with IL-6, IL-18, or both for 24 h, with corresponding quantification of fluorescence intensity. Scale Bar: 50μm. (F) ELISA results showing downregulation of extracellular HMOX2 in SimA9 cells following IL-18 treatment or IL-6/IL-18 co-treatment. Statistics: (A) unpaired t-test; (B, C) Spearman correlation analysis; (E, F) three independent experiments, one-way ANOVA followed by Tukey’s multiple comparisons test to assess differences among groups.

    Journal: bioRxiv

    Article Title: Hippocampal Neuroinflammation and Altered Peripheral Neurobiological Protein Profile in Experimental Arthritis and Systemic Juvenile Idiopathic Arthritis

    doi: 10.64898/2026.03.13.711607

    Figure Lengend Snippet: IL-6 and IL-18 are elevated in arthritic mice and synergistically trigger oxidative stress in microglia. (A) Box plots showing increased serum IL-6 and IL-18 levels in arthritic mice. (B) Correlation analysis showing a negative correlation between serum IL-18 and HMOX2, whereas IL-6 showed no significant correlation in arthritic mice. (C) Scatter plots showing the correlations between serum IL-18/IL-6 and microglial activation in arthritic mice. (D–E) Representative images of DCFH-DA staining showing ROS levels in SimA9 cells treated with IL-6, IL-18, or both for 24 h, with corresponding quantification of fluorescence intensity. Scale Bar: 50μm. (F) ELISA results showing downregulation of extracellular HMOX2 in SimA9 cells following IL-18 treatment or IL-6/IL-18 co-treatment. Statistics: (A) unpaired t-test; (B, C) Spearman correlation analysis; (E, F) three independent experiments, one-way ANOVA followed by Tukey’s multiple comparisons test to assess differences among groups.

    Article Snippet: Mouse serum samples were also used to measure IL-6 and IL-18 level using IL-6 and IL-18 mouse Elisa kits (R&D systems, USA).

    Techniques: Activation Assay, Staining, Fluorescence, Enzyme-linked Immunosorbent Assay