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inos production assay  (Elabscience Biotechnology)


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    Elabscience Biotechnology inos production assay
    Inos Production Assay, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/inos production assay/product/Elabscience Biotechnology
    Average 94 stars, based on 11 article reviews
    inos production assay - by Bioz Stars, 2026-06
    94/100 stars

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    IMP suppresses LPS‐induced NF‐κB activity and down‐regulates NF‐κB‐mediated pro‐inflammatory gene expression in LS174T cells. (A) HEK293T cells were transiently transfected with pGCL4.32 (luc2P/NF‐κB‐RE/Hygro) NF‐κB reporter, pCMV6‐entry or pCMV6‐XL4‐hPXR, and pRL‐TK. After transfection overnight, cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (RIF; 10 μM) for 24 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for another 24 h. A standard dual luciferase assay was performed on the cell lysates. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the TNF‐α group with or without hPXR. * P < 0.05 compared with the same treatment group transfected with empty vector and the TNF‐α group transfected with the receptor expression plasmid. (B) LS174T cells were treated with DMSO, IMP (25 μM) or rifampicin (10 μM) for 48 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for 24 h. NF‐κB p65 localization was performed using immunofluorescence staining and observed under a confocal laser scanning microscope (magnification: 630×) using an anti‐NF‐κB p65 antibody (1:50) followed by an Alexa Fluor 488‐conjugated detection antibody. (C) NF‐κB p65, phospho‐p65 (p‐p65), IκBα and phospho‐IκBα (p‐IκBα) protein levels in LS174T cells were determined by Western blotting. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (D) NF‐κB p65 protein levels in the cytoplasm and nucleus of LS174T cells were determined by Western blotting. GAPDH and PCNA were used as cytoplasm and nuclear markers respectively. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (E) The mRNA levels of IL‐1β, ICAM1, <t>iNOS</t> and COX‐2 were determined using qRT‐PCR. LS174T cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (10 μM) for 48 h, followed by additional exposure to LPS (2000 ng·mL−1) for 24 h. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the DMSO control group. * P < 0.05 compared with the LPS control group.
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    inos production assay  (Elabscience Biotechnology)
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    IMP suppresses LPS‐induced NF‐κB activity and down‐regulates NF‐κB‐mediated pro‐inflammatory gene expression in LS174T cells. (A) HEK293T cells were transiently transfected with pGCL4.32 (luc2P/NF‐κB‐RE/Hygro) NF‐κB reporter, pCMV6‐entry or pCMV6‐XL4‐hPXR, and pRL‐TK. After transfection overnight, cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (RIF; 10 μM) for 24 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for another 24 h. A standard dual luciferase assay was performed on the cell lysates. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the TNF‐α group with or without hPXR. * P < 0.05 compared with the same treatment group transfected with empty vector and the TNF‐α group transfected with the receptor expression plasmid. (B) LS174T cells were treated with DMSO, IMP (25 μM) or rifampicin (10 μM) for 48 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for 24 h. NF‐κB p65 localization was performed using immunofluorescence staining and observed under a confocal laser scanning microscope (magnification: 630×) using an anti‐NF‐κB p65 antibody (1:50) followed by an Alexa Fluor 488‐conjugated detection antibody. (C) NF‐κB p65, phospho‐p65 (p‐p65), IκBα and phospho‐IκBα (p‐IκBα) protein levels in LS174T cells were determined by Western blotting. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (D) NF‐κB p65 protein levels in the cytoplasm and nucleus of LS174T cells were determined by Western blotting. GAPDH and PCNA were used as cytoplasm and nuclear markers respectively. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (E) The mRNA levels of IL‐1β, ICAM1, <t>iNOS</t> and COX‐2 were determined using qRT‐PCR. LS174T cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (10 μM) for 48 h, followed by additional exposure to LPS (2000 ng·mL−1) for 24 h. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the DMSO control group. * P < 0.05 compared with the LPS control group.
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    inducible nitric oxide synthase inos production  (Galectin Therapeutics)
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    IMP suppresses LPS‐induced NF‐κB activity and down‐regulates NF‐κB‐mediated pro‐inflammatory gene expression in LS174T cells. (A) HEK293T cells were transiently transfected with pGCL4.32 (luc2P/NF‐κB‐RE/Hygro) NF‐κB reporter, pCMV6‐entry or pCMV6‐XL4‐hPXR, and pRL‐TK. After transfection overnight, cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (RIF; 10 μM) for 24 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for another 24 h. A standard dual luciferase assay was performed on the cell lysates. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the TNF‐α group with or without hPXR. * P < 0.05 compared with the same treatment group transfected with empty vector and the TNF‐α group transfected with the receptor expression plasmid. (B) LS174T cells were treated with DMSO, IMP (25 μM) or rifampicin (10 μM) for 48 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for 24 h. NF‐κB p65 localization was performed using immunofluorescence staining and observed under a confocal laser scanning microscope (magnification: 630×) using an anti‐NF‐κB p65 antibody (1:50) followed by an Alexa Fluor 488‐conjugated detection antibody. (C) NF‐κB p65, phospho‐p65 (p‐p65), IκBα and phospho‐IκBα (p‐IκBα) protein levels in LS174T cells were determined by Western blotting. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (D) NF‐κB p65 protein levels in the cytoplasm and nucleus of LS174T cells were determined by Western blotting. GAPDH and PCNA were used as cytoplasm and nuclear markers respectively. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (E) The mRNA levels of IL‐1β, ICAM1, <t>iNOS</t> and COX‐2 were determined using qRT‐PCR. LS174T cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (10 μM) for 48 h, followed by additional exposure to LPS (2000 ng·mL−1) for 24 h. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the DMSO control group. * P < 0.05 compared with the LPS control group.
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    IMP suppresses LPS‐induced NF‐κB activity and down‐regulates NF‐κB‐mediated pro‐inflammatory gene expression in LS174T cells. (A) HEK293T cells were transiently transfected with pGCL4.32 (luc2P/NF‐κB‐RE/Hygro) NF‐κB reporter, pCMV6‐entry or pCMV6‐XL4‐hPXR, and pRL‐TK. After transfection overnight, cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (RIF; 10 μM) for 24 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for another 24 h. A standard dual luciferase assay was performed on the cell lysates. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the TNF‐α group with or without hPXR. * P < 0.05 compared with the same treatment group transfected with empty vector and the TNF‐α group transfected with the receptor expression plasmid. (B) LS174T cells were treated with DMSO, IMP (25 μM) or rifampicin (10 μM) for 48 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for 24 h. NF‐κB p65 localization was performed using immunofluorescence staining and observed under a confocal laser scanning microscope (magnification: 630×) using an anti‐NF‐κB p65 antibody (1:50) followed by an Alexa Fluor 488‐conjugated detection antibody. (C) NF‐κB p65, phospho‐p65 (p‐p65), IκBα and phospho‐IκBα (p‐IκBα) protein levels in LS174T cells were determined by Western blotting. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (D) NF‐κB p65 protein levels in the cytoplasm and nucleus of LS174T cells were determined by Western blotting. GAPDH and PCNA were used as cytoplasm and nuclear markers respectively. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (E) The mRNA levels of IL‐1β, ICAM1, <t>iNOS</t> and COX‐2 were determined using qRT‐PCR. LS174T cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (10 μM) for 48 h, followed by additional exposure to LPS (2000 ng·mL−1) for 24 h. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the DMSO control group. * P < 0.05 compared with the LPS control group.
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    IMP suppresses LPS‐induced NF‐κB activity and down‐regulates NF‐κB‐mediated pro‐inflammatory gene expression in LS174T cells. (A) HEK293T cells were transiently transfected with pGCL4.32 (luc2P/NF‐κB‐RE/Hygro) NF‐κB reporter, pCMV6‐entry or pCMV6‐XL4‐hPXR, and pRL‐TK. After transfection overnight, cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (RIF; 10 μM) for 24 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for another 24 h. A standard dual luciferase assay was performed on the cell lysates. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the TNF‐α group with or without hPXR. * P < 0.05 compared with the same treatment group transfected with empty vector and the TNF‐α group transfected with the receptor expression plasmid. (B) LS174T cells were treated with DMSO, IMP (25 μM) or rifampicin (10 μM) for 48 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for 24 h. NF‐κB p65 localization was performed using immunofluorescence staining and observed under a confocal laser scanning microscope (magnification: 630×) using an anti‐NF‐κB p65 antibody (1:50) followed by an Alexa Fluor 488‐conjugated detection antibody. (C) NF‐κB p65, phospho‐p65 (p‐p65), IκBα and phospho‐IκBα (p‐IκBα) protein levels in LS174T cells were determined by Western blotting. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (D) NF‐κB p65 protein levels in the cytoplasm and nucleus of LS174T cells were determined by Western blotting. GAPDH and PCNA were used as cytoplasm and nuclear markers respectively. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (E) The mRNA levels of IL‐1β, ICAM1, <t>iNOS</t> and COX‐2 were determined using qRT‐PCR. LS174T cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (10 μM) for 48 h, followed by additional exposure to LPS (2000 ng·mL−1) for 24 h. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the DMSO control group. * P < 0.05 compared with the LPS control group.
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    inos production  (Cusabio)
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    IMP suppresses LPS‐induced NF‐κB activity and down‐regulates NF‐κB‐mediated pro‐inflammatory gene expression in LS174T cells. (A) HEK293T cells were transiently transfected with pGCL4.32 (luc2P/NF‐κB‐RE/Hygro) NF‐κB reporter, pCMV6‐entry or pCMV6‐XL4‐hPXR, and pRL‐TK. After transfection overnight, cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (RIF; 10 μM) for 24 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for another 24 h. A standard dual luciferase assay was performed on the cell lysates. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the TNF‐α group with or without hPXR. * P < 0.05 compared with the same treatment group transfected with empty vector and the TNF‐α group transfected with the receptor expression plasmid. (B) LS174T cells were treated with DMSO, IMP (25 μM) or rifampicin (10 μM) for 48 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for 24 h. NF‐κB p65 localization was performed using immunofluorescence staining and observed under a confocal laser scanning microscope (magnification: 630×) using an anti‐NF‐κB p65 antibody (1:50) followed by an Alexa Fluor 488‐conjugated detection antibody. (C) NF‐κB p65, phospho‐p65 (p‐p65), IκBα and phospho‐IκBα (p‐IκBα) protein levels in LS174T cells were determined by Western blotting. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (D) NF‐κB p65 protein levels in the cytoplasm and nucleus of LS174T cells were determined by Western blotting. GAPDH and PCNA were used as cytoplasm and nuclear markers respectively. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (E) The mRNA levels of IL‐1β, ICAM1, <t>iNOS</t> and COX‐2 were determined using qRT‐PCR. LS174T cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (10 μM) for 48 h, followed by additional exposure to LPS (2000 ng·mL−1) for 24 h. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the DMSO control group. * P < 0.05 compared with the LPS control group.
    Inos Production, supplied by Cusabio, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ino 4800 dna-based vaccination product  (Inovio Inc)
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    Inovio Inc ino 4800 dna-based vaccination product
    IMP suppresses LPS‐induced NF‐κB activity and down‐regulates NF‐κB‐mediated pro‐inflammatory gene expression in LS174T cells. (A) HEK293T cells were transiently transfected with pGCL4.32 (luc2P/NF‐κB‐RE/Hygro) NF‐κB reporter, pCMV6‐entry or pCMV6‐XL4‐hPXR, and pRL‐TK. After transfection overnight, cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (RIF; 10 μM) for 24 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for another 24 h. A standard dual luciferase assay was performed on the cell lysates. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the TNF‐α group with or without hPXR. * P < 0.05 compared with the same treatment group transfected with empty vector and the TNF‐α group transfected with the receptor expression plasmid. (B) LS174T cells were treated with DMSO, IMP (25 μM) or rifampicin (10 μM) for 48 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for 24 h. NF‐κB p65 localization was performed using immunofluorescence staining and observed under a confocal laser scanning microscope (magnification: 630×) using an anti‐NF‐κB p65 antibody (1:50) followed by an Alexa Fluor 488‐conjugated detection antibody. (C) NF‐κB p65, phospho‐p65 (p‐p65), IκBα and phospho‐IκBα (p‐IκBα) protein levels in LS174T cells were determined by Western blotting. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (D) NF‐κB p65 protein levels in the cytoplasm and nucleus of LS174T cells were determined by Western blotting. GAPDH and PCNA were used as cytoplasm and nuclear markers respectively. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (E) The mRNA levels of IL‐1β, ICAM1, <t>iNOS</t> and COX‐2 were determined using qRT‐PCR. LS174T cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (10 μM) for 48 h, followed by additional exposure to LPS (2000 ng·mL−1) for 24 h. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the DMSO control group. * P < 0.05 compared with the LPS control group.
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    nos2 activity (as total nitrite production by fluorometric assay;  (Cayman Chemical)
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    Cayman Chemical nos2 activity (as total nitrite production by fluorometric assay;
    IMP suppresses LPS‐induced NF‐κB activity and down‐regulates NF‐κB‐mediated pro‐inflammatory gene expression in LS174T cells. (A) HEK293T cells were transiently transfected with pGCL4.32 (luc2P/NF‐κB‐RE/Hygro) NF‐κB reporter, pCMV6‐entry or pCMV6‐XL4‐hPXR, and pRL‐TK. After transfection overnight, cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (RIF; 10 μM) for 24 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for another 24 h. A standard dual luciferase assay was performed on the cell lysates. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the TNF‐α group with or without hPXR. * P < 0.05 compared with the same treatment group transfected with empty vector and the TNF‐α group transfected with the receptor expression plasmid. (B) LS174T cells were treated with DMSO, IMP (25 μM) or rifampicin (10 μM) for 48 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for 24 h. NF‐κB p65 localization was performed using immunofluorescence staining and observed under a confocal laser scanning microscope (magnification: 630×) using an anti‐NF‐κB p65 antibody (1:50) followed by an Alexa Fluor 488‐conjugated detection antibody. (C) NF‐κB p65, phospho‐p65 (p‐p65), IκBα and phospho‐IκBα (p‐IκBα) protein levels in LS174T cells were determined by Western blotting. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (D) NF‐κB p65 protein levels in the cytoplasm and nucleus of LS174T cells were determined by Western blotting. GAPDH and PCNA were used as cytoplasm and nuclear markers respectively. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (E) The mRNA levels of IL‐1β, ICAM1, <t>iNOS</t> and COX‐2 were determined using qRT‐PCR. LS174T cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (10 μM) for 48 h, followed by additional exposure to LPS (2000 ng·mL−1) for 24 h. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the DMSO control group. * P < 0.05 compared with the LPS control group.
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    Image Search Results


    IMP suppresses LPS‐induced NF‐κB activity and down‐regulates NF‐κB‐mediated pro‐inflammatory gene expression in LS174T cells. (A) HEK293T cells were transiently transfected with pGCL4.32 (luc2P/NF‐κB‐RE/Hygro) NF‐κB reporter, pCMV6‐entry or pCMV6‐XL4‐hPXR, and pRL‐TK. After transfection overnight, cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (RIF; 10 μM) for 24 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for another 24 h. A standard dual luciferase assay was performed on the cell lysates. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the TNF‐α group with or without hPXR. * P < 0.05 compared with the same treatment group transfected with empty vector and the TNF‐α group transfected with the receptor expression plasmid. (B) LS174T cells were treated with DMSO, IMP (25 μM) or rifampicin (10 μM) for 48 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for 24 h. NF‐κB p65 localization was performed using immunofluorescence staining and observed under a confocal laser scanning microscope (magnification: 630×) using an anti‐NF‐κB p65 antibody (1:50) followed by an Alexa Fluor 488‐conjugated detection antibody. (C) NF‐κB p65, phospho‐p65 (p‐p65), IκBα and phospho‐IκBα (p‐IκBα) protein levels in LS174T cells were determined by Western blotting. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (D) NF‐κB p65 protein levels in the cytoplasm and nucleus of LS174T cells were determined by Western blotting. GAPDH and PCNA were used as cytoplasm and nuclear markers respectively. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (E) The mRNA levels of IL‐1β, ICAM1, iNOS and COX‐2 were determined using qRT‐PCR. LS174T cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (10 μM) for 48 h, followed by additional exposure to LPS (2000 ng·mL−1) for 24 h. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the DMSO control group. * P < 0.05 compared with the LPS control group.

    Journal: British Journal of Pharmacology

    Article Title: Activating the pregnane X receptor by imperatorin attenuates dextran sulphate sodium‐induced colitis in mice

    doi: 10.1111/bph.14424

    Figure Lengend Snippet: IMP suppresses LPS‐induced NF‐κB activity and down‐regulates NF‐κB‐mediated pro‐inflammatory gene expression in LS174T cells. (A) HEK293T cells were transiently transfected with pGCL4.32 (luc2P/NF‐κB‐RE/Hygro) NF‐κB reporter, pCMV6‐entry or pCMV6‐XL4‐hPXR, and pRL‐TK. After transfection overnight, cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (RIF; 10 μM) for 24 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for another 24 h. A standard dual luciferase assay was performed on the cell lysates. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the TNF‐α group with or without hPXR. * P < 0.05 compared with the same treatment group transfected with empty vector and the TNF‐α group transfected with the receptor expression plasmid. (B) LS174T cells were treated with DMSO, IMP (25 μM) or rifampicin (10 μM) for 48 h, followed by additional incubation with or without TNF‐α (20 ng·mL−1) for 24 h. NF‐κB p65 localization was performed using immunofluorescence staining and observed under a confocal laser scanning microscope (magnification: 630×) using an anti‐NF‐κB p65 antibody (1:50) followed by an Alexa Fluor 488‐conjugated detection antibody. (C) NF‐κB p65, phospho‐p65 (p‐p65), IκBα and phospho‐IκBα (p‐IκBα) protein levels in LS174T cells were determined by Western blotting. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (D) NF‐κB p65 protein levels in the cytoplasm and nucleus of LS174T cells were determined by Western blotting. GAPDH and PCNA were used as cytoplasm and nuclear markers respectively. The numbers at the bottom indicate the relative intensity of the protein bands, with the DMSO‐treated sample set as ‘1.00’. (E) The mRNA levels of IL‐1β, ICAM1, iNOS and COX‐2 were determined using qRT‐PCR. LS174T cells were treated with DMSO, IMP (6.25–25 μM) or rifampicin (10 μM) for 48 h, followed by additional exposure to LPS (2000 ng·mL−1) for 24 h. Results are expressed as fold changes compared with the DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with the DMSO control group. * P < 0.05 compared with the LPS control group.

    Article Snippet: The following TaqMan probes were used: hPXR ( https://www.thermofisher.com/taqman-gene-expression/product/Hs01114267_m1?CID=&ICID=&subtype= , Mm01344139_m1), CYP3A4 ( https://www.thermofisher.com/taqman-gene-expression/product/Hs00604506_m1?CID=&ICID=&subtype= ), Cyp3a11 (Mm00731567_m1), MDR1 ( https://www.thermofisher.com/taqman-gene-expression/product/Hs00184500_m1?CID=&ICID=&subtype= , Mm00440761_m1), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4974 ( https://www.thermofisher.com/taqman-gene-expression/product/Hs01555410_m1?CID=&ICID=&subtype= ), iNOS ( https://www.thermofisher.com/taqman-gene-expression/product/Hs01075529_m1?CID=&ICID=&subtype= ), COX‐2 ( https://www.thermofisher.com/taqman-gene-expression/product/Hs00153133_m1?CID=&ICID=&subtype= ), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=6757 ( https://www.thermofisher.com/taqman-gene-expression/product/Hs00164932_m1?CID=&ICID=&subtype= ) and GAPDH ( https://www.thermofisher.com/taqman-gene-expression/product/Hs02786624_g1?CID=&ICID=&subtype= , Mm99999915_g1).

    Techniques: Activity Assay, Expressing, Transfection, Incubation, Luciferase, Plasmid Preparation, Immunofluorescence, Staining, Laser-Scanning Microscopy, Western Blot, Quantitative RT-PCR

    Knockdown of hPXR attenuated IMP‐mediated suppression of pro‐inflammatory gene expression in LS174T cells. (A) Cells were transiently transfected with hPXR siRNA and control non‐silencing siRNA. After transfection for 48 h, the cells were treated with DMSO, IMP (25 μM) or rifampicin (RIF; 10 μM) for another 48 h, followed by additional exposure to LPS (2000 ng·mL−1) for 24 h. The mRNA expression levels of IL‐1β, ICAM1, iNOS and COX‐2 were determined by qRT‐PCR. Results are expressed as fold changes compared with DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with DMSO group. * P < 0.05 compared with the same treatment group. (B) LS174T cells were transiently transfected with hPXR siRNA and control non‐silencing siRNA for 24 h and then treated with DMSO, IMP (25 μM) or rifampicin (10 μM) for another 48 h, followed by an additional incubation with or without TNF‐α (20 ng·mL−1) for 24 h. NF‐κB p65 localization was performed using immunofluorescence staining and observed under a confocal laser scanning microscope (magnification: 630×) using an anti‐NF‐κB p65 antibody (1:50) followed by an Alexa Fluor 488‐conjugated detection antibody.

    Journal: British Journal of Pharmacology

    Article Title: Activating the pregnane X receptor by imperatorin attenuates dextran sulphate sodium‐induced colitis in mice

    doi: 10.1111/bph.14424

    Figure Lengend Snippet: Knockdown of hPXR attenuated IMP‐mediated suppression of pro‐inflammatory gene expression in LS174T cells. (A) Cells were transiently transfected with hPXR siRNA and control non‐silencing siRNA. After transfection for 48 h, the cells were treated with DMSO, IMP (25 μM) or rifampicin (RIF; 10 μM) for another 48 h, followed by additional exposure to LPS (2000 ng·mL−1) for 24 h. The mRNA expression levels of IL‐1β, ICAM1, iNOS and COX‐2 were determined by qRT‐PCR. Results are expressed as fold changes compared with DMSO control. Data are expressed as mean ± SEM from five independent experiments. # P < 0.05 compared with DMSO group. * P < 0.05 compared with the same treatment group. (B) LS174T cells were transiently transfected with hPXR siRNA and control non‐silencing siRNA for 24 h and then treated with DMSO, IMP (25 μM) or rifampicin (10 μM) for another 48 h, followed by an additional incubation with or without TNF‐α (20 ng·mL−1) for 24 h. NF‐κB p65 localization was performed using immunofluorescence staining and observed under a confocal laser scanning microscope (magnification: 630×) using an anti‐NF‐κB p65 antibody (1:50) followed by an Alexa Fluor 488‐conjugated detection antibody.

    Article Snippet: The following TaqMan probes were used: hPXR ( https://www.thermofisher.com/taqman-gene-expression/product/Hs01114267_m1?CID=&ICID=&subtype= , Mm01344139_m1), CYP3A4 ( https://www.thermofisher.com/taqman-gene-expression/product/Hs00604506_m1?CID=&ICID=&subtype= ), Cyp3a11 (Mm00731567_m1), MDR1 ( https://www.thermofisher.com/taqman-gene-expression/product/Hs00184500_m1?CID=&ICID=&subtype= , Mm00440761_m1), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4974 ( https://www.thermofisher.com/taqman-gene-expression/product/Hs01555410_m1?CID=&ICID=&subtype= ), iNOS ( https://www.thermofisher.com/taqman-gene-expression/product/Hs01075529_m1?CID=&ICID=&subtype= ), COX‐2 ( https://www.thermofisher.com/taqman-gene-expression/product/Hs00153133_m1?CID=&ICID=&subtype= ), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=6757 ( https://www.thermofisher.com/taqman-gene-expression/product/Hs00164932_m1?CID=&ICID=&subtype= ) and GAPDH ( https://www.thermofisher.com/taqman-gene-expression/product/Hs02786624_g1?CID=&ICID=&subtype= , Mm99999915_g1).

    Techniques: Expressing, Transfection, Quantitative RT-PCR, Incubation, Immunofluorescence, Staining, Laser-Scanning Microscopy