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cell culture thp1 blue nf κb monocytes  (InvivoGen)


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    InvivoGen cell culture thp1 blue nf κb monocytes
    <t>NF-κB</t> activation by air pollution PMs. (A) Schema of NF-κB activation in the <t>THP1-Blue</t> monocyte assay; (B) NF-κB activation by 24 h (nPM and sPM, 5 μg/ml; DEP, 100 μg/ml; LPS, 10 ng/ml). (C) LPS neutralization by pretreatment with polymyxin B (10 ng/ml, 20 min) before NF-κB activation by nPM or sPM (5 μg/ml/24 h). * Adjusted p-value < 0.05, N = 4.
    Cell Culture Thp1 Blue Nf κb Monocytes, supplied by InvivoGen, used in various techniques. Bioz Stars score: 96/100, based on 190 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cell culture thp1 blue nf κb monocytes/product/InvivoGen
    Average 96 stars, based on 190 article reviews
    cell culture thp1 blue nf κb monocytes - by Bioz Stars, 2026-03
    96/100 stars

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    1) Product Images from "Cell-based assays that predict in vivo neurotoxicity of urban ambient nanosized particulate matter"

    Article Title: Cell-based assays that predict in vivo neurotoxicity of urban ambient nanosized particulate matter

    Journal: Free radical biology & medicine

    doi: 10.1016/j.freeradbiomed.2019.09.016

    NF-κB activation by air pollution PMs. (A) Schema of NF-κB activation in the THP1-Blue monocyte assay; (B) NF-κB activation by 24 h (nPM and sPM, 5 μg/ml; DEP, 100 μg/ml; LPS, 10 ng/ml). (C) LPS neutralization by pretreatment with polymyxin B (10 ng/ml, 20 min) before NF-κB activation by nPM or sPM (5 μg/ml/24 h). * Adjusted p-value < 0.05, N = 4.
    Figure Legend Snippet: NF-κB activation by air pollution PMs. (A) Schema of NF-κB activation in the THP1-Blue monocyte assay; (B) NF-κB activation by 24 h (nPM and sPM, 5 μg/ml; DEP, 100 μg/ml; LPS, 10 ng/ml). (C) LPS neutralization by pretreatment with polymyxin B (10 ng/ml, 20 min) before NF-κB activation by nPM or sPM (5 μg/ml/24 h). * Adjusted p-value < 0.05, N = 4.

    Techniques Used: Activation Assay, Neutralization

    nPM induced cytokines through NF-κB activation in THP1 monocytes. (A) nPM increased nuclear NF-κB p65 (Western blot) by 5 μg/ml nPM (B) Cytokine induction by nPM (RT-PCR) was suppressed by pretreatment with 40 μg/ml of SN50, a NF-κB inhibitor. *P < 0.05, **P < 0.01 vs control, #, P < 0.05, nPM alone, N = 4.
    Figure Legend Snippet: nPM induced cytokines through NF-κB activation in THP1 monocytes. (A) nPM increased nuclear NF-κB p65 (Western blot) by 5 μg/ml nPM (B) Cytokine induction by nPM (RT-PCR) was suppressed by pretreatment with 40 μg/ml of SN50, a NF-κB inhibitor. *P < 0.05, **P < 0.01 vs control, #, P < 0.05, nPM alone, N = 4.

    Techniques Used: Activation Assay, Western Blot, Reverse Transcription Polymerase Chain Reaction

    Lipid peroxidation potency measured by DPPP assay. After incubation with DPPP (4.5 μM/15min), THP1-Blue cells were exposed to air pollution PM (nPM, sPM, DEP: 10 μg/ml), LPS (10 μg/ml), or H2O2 (200 μM) for 20 min, and fluorescence was measured (excitation, 351 nm; emission, 380 nm). * p-value < 0.05, N = 4.
    Figure Legend Snippet: Lipid peroxidation potency measured by DPPP assay. After incubation with DPPP (4.5 μM/15min), THP1-Blue cells were exposed to air pollution PM (nPM, sPM, DEP: 10 μg/ml), LPS (10 μg/ml), or H2O2 (200 μM) for 20 min, and fluorescence was measured (excitation, 351 nm; emission, 380 nm). * p-value < 0.05, N = 4.

    Techniques Used: Incubation, Fluorescence

    In vivo neurotoxic responses of nPM paralleled in vitro NF-κB induction activity. Young male mice were exposed for 3 or 8 weeks to nPM batches with different in vitro NF-κB activity for neurotoxic responses. A) Inflammatory cytokines after 3 weeks of exposure to 300 μg/m3 of PM0.2. Heatmap shows the fold changes of inflammatory cytokines in mice exposed to particles vs controls exposed to filtered air. B) In vitro NF-κB activation potency of PM was associated with the variance of cerebral cortex inflammatory responses. Principal component analysis of the 9 inflammatory cytokines was calculated for each mouse. In vitro NF-κB response was associated with PC3 that explained 17% of the variance brain inflammatory response. Cerebral cortex inflammatory profile of mice exposed to different batches of nPM or sPM did not correlate with in vitro (C) lipid peroxidation or (D) NO production. E) nPM with stronger NF-κB activation in vitro caused more increase in cerebral cortex amyloid-β40 &-42 peptides and hippocampal Iba1. Mean ± SEM. * adjusted P-values < 0.05. N = 5–10/group.
    Figure Legend Snippet: In vivo neurotoxic responses of nPM paralleled in vitro NF-κB induction activity. Young male mice were exposed for 3 or 8 weeks to nPM batches with different in vitro NF-κB activity for neurotoxic responses. A) Inflammatory cytokines after 3 weeks of exposure to 300 μg/m3 of PM0.2. Heatmap shows the fold changes of inflammatory cytokines in mice exposed to particles vs controls exposed to filtered air. B) In vitro NF-κB activation potency of PM was associated with the variance of cerebral cortex inflammatory responses. Principal component analysis of the 9 inflammatory cytokines was calculated for each mouse. In vitro NF-κB response was associated with PC3 that explained 17% of the variance brain inflammatory response. Cerebral cortex inflammatory profile of mice exposed to different batches of nPM or sPM did not correlate with in vitro (C) lipid peroxidation or (D) NO production. E) nPM with stronger NF-κB activation in vitro caused more increase in cerebral cortex amyloid-β40 &-42 peptides and hippocampal Iba1. Mean ± SEM. * adjusted P-values < 0.05. N = 5–10/group.

    Techniques Used: In Vivo, In Vitro, Activity Assay, Activation Assay



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    <t>NF-κB</t> activation by air pollution PMs. (A) Schema of NF-κB activation in the <t>THP1-Blue</t> monocyte assay; (B) NF-κB activation by 24 h (nPM and sPM, 5 μg/ml; DEP, 100 μg/ml; LPS, 10 ng/ml). (C) LPS neutralization by pretreatment with polymyxin B (10 ng/ml, 20 min) before NF-κB activation by nPM or sPM (5 μg/ml/24 h). * Adjusted p-value < 0.05, N = 4.
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    cell culture human monocytic thp 1blue cells  (InvivoGen)
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    <t>NF-κB</t> activation by air pollution PMs. (A) Schema of NF-κB activation in the <t>THP1-Blue</t> monocyte assay; (B) NF-κB activation by 24 h (nPM and sPM, 5 μg/ml; DEP, 100 μg/ml; LPS, 10 ng/ml). (C) LPS neutralization by pretreatment with polymyxin B (10 ng/ml, 20 min) before NF-κB activation by nPM or sPM (5 μg/ml/24 h). * Adjusted p-value < 0.05, N = 4.
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    Image Search Results


    NF-κB activation by air pollution PMs. (A) Schema of NF-κB activation in the THP1-Blue monocyte assay; (B) NF-κB activation by 24 h (nPM and sPM, 5 μg/ml; DEP, 100 μg/ml; LPS, 10 ng/ml). (C) LPS neutralization by pretreatment with polymyxin B (10 ng/ml, 20 min) before NF-κB activation by nPM or sPM (5 μg/ml/24 h). * Adjusted p-value < 0.05, N = 4.

    Journal: Free radical biology & medicine

    Article Title: Cell-based assays that predict in vivo neurotoxicity of urban ambient nanosized particulate matter

    doi: 10.1016/j.freeradbiomed.2019.09.016

    Figure Lengend Snippet: NF-κB activation by air pollution PMs. (A) Schema of NF-κB activation in the THP1-Blue monocyte assay; (B) NF-κB activation by 24 h (nPM and sPM, 5 μg/ml; DEP, 100 μg/ml; LPS, 10 ng/ml). (C) LPS neutralization by pretreatment with polymyxin B (10 ng/ml, 20 min) before NF-κB activation by nPM or sPM (5 μg/ml/24 h). * Adjusted p-value < 0.05, N = 4.

    Article Snippet: Cell culture THP1-Blue NF-κB monocytes from InvivoGen (San Diego, CA, USA) were maintained in RPMI1640 medium containing 10% FBS, 1% pen/strep, 100 μg/ml Normocin, and 10 μg/ml Blasticidin at 4×10 5 −1×10 6 cells/ml with 5% CO 2 at 37 °C.

    Techniques: Activation Assay, Neutralization

    nPM induced cytokines through NF-κB activation in THP1 monocytes. (A) nPM increased nuclear NF-κB p65 (Western blot) by 5 μg/ml nPM (B) Cytokine induction by nPM (RT-PCR) was suppressed by pretreatment with 40 μg/ml of SN50, a NF-κB inhibitor. *P < 0.05, **P < 0.01 vs control, #, P < 0.05, nPM alone, N = 4.

    Journal: Free radical biology & medicine

    Article Title: Cell-based assays that predict in vivo neurotoxicity of urban ambient nanosized particulate matter

    doi: 10.1016/j.freeradbiomed.2019.09.016

    Figure Lengend Snippet: nPM induced cytokines through NF-κB activation in THP1 monocytes. (A) nPM increased nuclear NF-κB p65 (Western blot) by 5 μg/ml nPM (B) Cytokine induction by nPM (RT-PCR) was suppressed by pretreatment with 40 μg/ml of SN50, a NF-κB inhibitor. *P < 0.05, **P < 0.01 vs control, #, P < 0.05, nPM alone, N = 4.

    Article Snippet: Cell culture THP1-Blue NF-κB monocytes from InvivoGen (San Diego, CA, USA) were maintained in RPMI1640 medium containing 10% FBS, 1% pen/strep, 100 μg/ml Normocin, and 10 μg/ml Blasticidin at 4×10 5 −1×10 6 cells/ml with 5% CO 2 at 37 °C.

    Techniques: Activation Assay, Western Blot, Reverse Transcription Polymerase Chain Reaction

    Lipid peroxidation potency measured by DPPP assay. After incubation with DPPP (4.5 μM/15min), THP1-Blue cells were exposed to air pollution PM (nPM, sPM, DEP: 10 μg/ml), LPS (10 μg/ml), or H2O2 (200 μM) for 20 min, and fluorescence was measured (excitation, 351 nm; emission, 380 nm). * p-value < 0.05, N = 4.

    Journal: Free radical biology & medicine

    Article Title: Cell-based assays that predict in vivo neurotoxicity of urban ambient nanosized particulate matter

    doi: 10.1016/j.freeradbiomed.2019.09.016

    Figure Lengend Snippet: Lipid peroxidation potency measured by DPPP assay. After incubation with DPPP (4.5 μM/15min), THP1-Blue cells were exposed to air pollution PM (nPM, sPM, DEP: 10 μg/ml), LPS (10 μg/ml), or H2O2 (200 μM) for 20 min, and fluorescence was measured (excitation, 351 nm; emission, 380 nm). * p-value < 0.05, N = 4.

    Article Snippet: Cell culture THP1-Blue NF-κB monocytes from InvivoGen (San Diego, CA, USA) were maintained in RPMI1640 medium containing 10% FBS, 1% pen/strep, 100 μg/ml Normocin, and 10 μg/ml Blasticidin at 4×10 5 −1×10 6 cells/ml with 5% CO 2 at 37 °C.

    Techniques: Incubation, Fluorescence

    In vivo neurotoxic responses of nPM paralleled in vitro NF-κB induction activity. Young male mice were exposed for 3 or 8 weeks to nPM batches with different in vitro NF-κB activity for neurotoxic responses. A) Inflammatory cytokines after 3 weeks of exposure to 300 μg/m3 of PM0.2. Heatmap shows the fold changes of inflammatory cytokines in mice exposed to particles vs controls exposed to filtered air. B) In vitro NF-κB activation potency of PM was associated with the variance of cerebral cortex inflammatory responses. Principal component analysis of the 9 inflammatory cytokines was calculated for each mouse. In vitro NF-κB response was associated with PC3 that explained 17% of the variance brain inflammatory response. Cerebral cortex inflammatory profile of mice exposed to different batches of nPM or sPM did not correlate with in vitro (C) lipid peroxidation or (D) NO production. E) nPM with stronger NF-κB activation in vitro caused more increase in cerebral cortex amyloid-β40 &-42 peptides and hippocampal Iba1. Mean ± SEM. * adjusted P-values < 0.05. N = 5–10/group.

    Journal: Free radical biology & medicine

    Article Title: Cell-based assays that predict in vivo neurotoxicity of urban ambient nanosized particulate matter

    doi: 10.1016/j.freeradbiomed.2019.09.016

    Figure Lengend Snippet: In vivo neurotoxic responses of nPM paralleled in vitro NF-κB induction activity. Young male mice were exposed for 3 or 8 weeks to nPM batches with different in vitro NF-κB activity for neurotoxic responses. A) Inflammatory cytokines after 3 weeks of exposure to 300 μg/m3 of PM0.2. Heatmap shows the fold changes of inflammatory cytokines in mice exposed to particles vs controls exposed to filtered air. B) In vitro NF-κB activation potency of PM was associated with the variance of cerebral cortex inflammatory responses. Principal component analysis of the 9 inflammatory cytokines was calculated for each mouse. In vitro NF-κB response was associated with PC3 that explained 17% of the variance brain inflammatory response. Cerebral cortex inflammatory profile of mice exposed to different batches of nPM or sPM did not correlate with in vitro (C) lipid peroxidation or (D) NO production. E) nPM with stronger NF-κB activation in vitro caused more increase in cerebral cortex amyloid-β40 &-42 peptides and hippocampal Iba1. Mean ± SEM. * adjusted P-values < 0.05. N = 5–10/group.

    Article Snippet: Cell culture THP1-Blue NF-κB monocytes from InvivoGen (San Diego, CA, USA) were maintained in RPMI1640 medium containing 10% FBS, 1% pen/strep, 100 μg/ml Normocin, and 10 μg/ml Blasticidin at 4×10 5 −1×10 6 cells/ml with 5% CO 2 at 37 °C.

    Techniques: In Vivo, In Vitro, Activity Assay, Activation Assay