hil experiment Search Results


85
Thermo Fisher gene exp entpd2 mm00515450 m1
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MathWorks Inc hil experiment
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R&D Systems anti human il 12 moab
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R&D Systems monoclonal anti human il 4
Monoclonal Anti Human Il 4, supplied by R&D Systems, 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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R&D Systems human il 6 quantikine elisa kit
Human Il 6 Quantikine Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ImmunoTools recombinant hil-6
Recombinant Hil 6, supplied by ImmunoTools, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Human Il 6, supplied by ProSpec, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Hermetia Baruth chitin binding cuticle protein hil g2 068406 hermetia
Chitin Binding Cuticle Protein Hil G2 068406 Hermetia, supplied by Hermetia Baruth, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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R&D Systems anti human il 6 antibody
In vitro evaluation of monocyte-derived cytokine signaling on CEA expression in colorectal cancer cells. (A) Schematic diagram of the experimental workflow. THP-1 monocytes were exposed to amorphous silica (SiO 2 ) and treated with NF-κB inhibitor (BAY 11-7082) <t>or</t> <t>IL-6</t> neutralizing antibody. Conditioned media (CM) were collected and applied to colorectal cancer cell lines (HT29 and Caco-2) to evaluate CEA mRNA and protein expression. (B) RT-qPCR quantification of IL-6, IL-1β, and TNF-α mRNA expression in THP-1 cells following low/high-dose SiO 2 stimulation with or without BAY 11–7082 treatment. (C) CEA mRNA and protein levels in HT29 and Caco-2 cells directly treated with SiO 2 particles (without conditioned media exposure). (D) CEA mRNA and protein expression in HT29 and Caco-2 cells treated with conditioned media derived from silica-stimulated THP-1 cells, with or without IL-6 neutralization or NF-κB inhibition. (E) CEA mRNA and protein levels in colorectal cancer cells treated with CM under varying conditions: anti-IL-6 antibody, NF-κB inhibitor (BAY 11-7082), or both. Statistical comparisons are shown between multiple experimental groups. Significance levels: P < 0.05 (*), P < 0.01 (**), P < 0.001 (***), P < 0.0001 (****).
Anti Human Il 6 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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OPAL-RT Technologies Inc hil realtime simulator
In vitro evaluation of monocyte-derived cytokine signaling on CEA expression in colorectal cancer cells. (A) Schematic diagram of the experimental workflow. THP-1 monocytes were exposed to amorphous silica (SiO 2 ) and treated with NF-κB inhibitor (BAY 11-7082) <t>or</t> <t>IL-6</t> neutralizing antibody. Conditioned media (CM) were collected and applied to colorectal cancer cell lines (HT29 and Caco-2) to evaluate CEA mRNA and protein expression. (B) RT-qPCR quantification of IL-6, IL-1β, and TNF-α mRNA expression in THP-1 cells following low/high-dose SiO 2 stimulation with or without BAY 11–7082 treatment. (C) CEA mRNA and protein levels in HT29 and Caco-2 cells directly treated with SiO 2 particles (without conditioned media exposure). (D) CEA mRNA and protein expression in HT29 and Caco-2 cells treated with conditioned media derived from silica-stimulated THP-1 cells, with or without IL-6 neutralization or NF-κB inhibition. (E) CEA mRNA and protein levels in colorectal cancer cells treated with CM under varying conditions: anti-IL-6 antibody, NF-κB inhibitor (BAY 11-7082), or both. Statistical comparisons are shown between multiple experimental groups. Significance levels: P < 0.05 (*), P < 0.01 (**), P < 0.001 (***), P < 0.0001 (****).
Hil Realtime Simulator, supplied by OPAL-RT Technologies Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94
Abcam human il 6 elisa kit
CMP treatment reduces ARPE-19 inflammatory signaling: <t>ELISA</t> measurements. ( A ) <t>Interleukin-6</t> <t>(IL-6)</t> secretion from ARPE-19 cells increased significantly following treatment with activated MMP-1 (60 nM) for 6 h compared to intact collagen control (#, p < 0.001). Following a complete exchange of media, cells were treated with 200 µM CMP 13A, which reduced Il-6 by 5-fold (*, p = 0.007) to control levels ( p = 0.99). Right: positive control using lipopolysaccharide (LPS, 10 mg/mL) shows +30-fold increase compared to control ( p <0.001). ( B ) Left: IL-6 secretion increased significantly following 24 h of 20 nM MMP-1 (#, p < 0.001). Concurrent treatment with CMP 13A significantly reduced Il-6 compared to MMP-1 ( p = 0.005), as did a combination of CMP 13A and 03A ( p = 0.014, concentration of each was 200 µM). Right: adding 200 µM CMP 13A at the 12 h mark for the remaining 12 h also reduced Il-6 compared to MMP-1 ( p = 0.001). ( C ) Interleukin-8 (IL-8) secretion from ARPE-19 cells also increased following MMP-1(6 h, 60 nM) compared to control (#, p < 0.001). Following complete media exchange, CMP 13A reduced Il-8 compared to both MMP-1 and control (*, p < 0.001). LPS positive control (right) induced a nearly 30-fold increase in IL-8 compared to control (#, p < 0.001). ( D ) IL-8 secretion did not change following 24 h of 20 nM MMP-1 alone or with concurrent treatment with CMP compared to control ( p = 0.30). For each measurement, n ≥ 6.
Human Il 6 Elisa Kit, supplied by Abcam, 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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Thermo Fisher gene exp il2 hs00174114 m1
CMP treatment reduces ARPE-19 inflammatory signaling: <t>ELISA</t> measurements. ( A ) <t>Interleukin-6</t> <t>(IL-6)</t> secretion from ARPE-19 cells increased significantly following treatment with activated MMP-1 (60 nM) for 6 h compared to intact collagen control (#, p < 0.001). Following a complete exchange of media, cells were treated with 200 µM CMP 13A, which reduced Il-6 by 5-fold (*, p = 0.007) to control levels ( p = 0.99). Right: positive control using lipopolysaccharide (LPS, 10 mg/mL) shows +30-fold increase compared to control ( p <0.001). ( B ) Left: IL-6 secretion increased significantly following 24 h of 20 nM MMP-1 (#, p < 0.001). Concurrent treatment with CMP 13A significantly reduced Il-6 compared to MMP-1 ( p = 0.005), as did a combination of CMP 13A and 03A ( p = 0.014, concentration of each was 200 µM). Right: adding 200 µM CMP 13A at the 12 h mark for the remaining 12 h also reduced Il-6 compared to MMP-1 ( p = 0.001). ( C ) Interleukin-8 (IL-8) secretion from ARPE-19 cells also increased following MMP-1(6 h, 60 nM) compared to control (#, p < 0.001). Following complete media exchange, CMP 13A reduced Il-8 compared to both MMP-1 and control (*, p < 0.001). LPS positive control (right) induced a nearly 30-fold increase in IL-8 compared to control (#, p < 0.001). ( D ) IL-8 secretion did not change following 24 h of 20 nM MMP-1 alone or with concurrent treatment with CMP compared to control ( p = 0.30). For each measurement, n ≥ 6.
Gene Exp Il2 Hs00174114 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


In vitro evaluation of monocyte-derived cytokine signaling on CEA expression in colorectal cancer cells. (A) Schematic diagram of the experimental workflow. THP-1 monocytes were exposed to amorphous silica (SiO 2 ) and treated with NF-κB inhibitor (BAY 11-7082) or IL-6 neutralizing antibody. Conditioned media (CM) were collected and applied to colorectal cancer cell lines (HT29 and Caco-2) to evaluate CEA mRNA and protein expression. (B) RT-qPCR quantification of IL-6, IL-1β, and TNF-α mRNA expression in THP-1 cells following low/high-dose SiO 2 stimulation with or without BAY 11–7082 treatment. (C) CEA mRNA and protein levels in HT29 and Caco-2 cells directly treated with SiO 2 particles (without conditioned media exposure). (D) CEA mRNA and protein expression in HT29 and Caco-2 cells treated with conditioned media derived from silica-stimulated THP-1 cells, with or without IL-6 neutralization or NF-κB inhibition. (E) CEA mRNA and protein levels in colorectal cancer cells treated with CM under varying conditions: anti-IL-6 antibody, NF-κB inhibitor (BAY 11-7082), or both. Statistical comparisons are shown between multiple experimental groups. Significance levels: P < 0.05 (*), P < 0.01 (**), P < 0.001 (***), P < 0.0001 (****).

Journal: Frontiers in Immunology

Article Title: Occupational silica exposure drives systemic immune dysregulation and tumor microenvironment susceptibility: evidence from a real-world study

doi: 10.3389/fimmu.2026.1775236

Figure Lengend Snippet: In vitro evaluation of monocyte-derived cytokine signaling on CEA expression in colorectal cancer cells. (A) Schematic diagram of the experimental workflow. THP-1 monocytes were exposed to amorphous silica (SiO 2 ) and treated with NF-κB inhibitor (BAY 11-7082) or IL-6 neutralizing antibody. Conditioned media (CM) were collected and applied to colorectal cancer cell lines (HT29 and Caco-2) to evaluate CEA mRNA and protein expression. (B) RT-qPCR quantification of IL-6, IL-1β, and TNF-α mRNA expression in THP-1 cells following low/high-dose SiO 2 stimulation with or without BAY 11–7082 treatment. (C) CEA mRNA and protein levels in HT29 and Caco-2 cells directly treated with SiO 2 particles (without conditioned media exposure). (D) CEA mRNA and protein expression in HT29 and Caco-2 cells treated with conditioned media derived from silica-stimulated THP-1 cells, with or without IL-6 neutralization or NF-κB inhibition. (E) CEA mRNA and protein levels in colorectal cancer cells treated with CM under varying conditions: anti-IL-6 antibody, NF-κB inhibitor (BAY 11-7082), or both. Statistical comparisons are shown between multiple experimental groups. Significance levels: P < 0.05 (*), P < 0.01 (**), P < 0.001 (***), P < 0.0001 (****).

Article Snippet: For IL-6 neutralization experiments, a monoclonal anti-human IL-6 antibody (R&D Systems, MAB206) was added at a final concentration of 2 μg/mL at the onset of stimulation.

Techniques: In Vitro, Derivative Assay, Expressing, Quantitative RT-PCR, Neutralization, Inhibition

CMP treatment reduces ARPE-19 inflammatory signaling: ELISA measurements. ( A ) Interleukin-6 (IL-6) secretion from ARPE-19 cells increased significantly following treatment with activated MMP-1 (60 nM) for 6 h compared to intact collagen control (#, p < 0.001). Following a complete exchange of media, cells were treated with 200 µM CMP 13A, which reduced Il-6 by 5-fold (*, p = 0.007) to control levels ( p = 0.99). Right: positive control using lipopolysaccharide (LPS, 10 mg/mL) shows +30-fold increase compared to control ( p <0.001). ( B ) Left: IL-6 secretion increased significantly following 24 h of 20 nM MMP-1 (#, p < 0.001). Concurrent treatment with CMP 13A significantly reduced Il-6 compared to MMP-1 ( p = 0.005), as did a combination of CMP 13A and 03A ( p = 0.014, concentration of each was 200 µM). Right: adding 200 µM CMP 13A at the 12 h mark for the remaining 12 h also reduced Il-6 compared to MMP-1 ( p = 0.001). ( C ) Interleukin-8 (IL-8) secretion from ARPE-19 cells also increased following MMP-1(6 h, 60 nM) compared to control (#, p < 0.001). Following complete media exchange, CMP 13A reduced Il-8 compared to both MMP-1 and control (*, p < 0.001). LPS positive control (right) induced a nearly 30-fold increase in IL-8 compared to control (#, p < 0.001). ( D ) IL-8 secretion did not change following 24 h of 20 nM MMP-1 alone or with concurrent treatment with CMP compared to control ( p = 0.30). For each measurement, n ≥ 6.

Journal: International Journal of Molecular Sciences

Article Title: Collagen Mimetic Peptides Promote Adherence and Migration of ARPE-19 Cells While Reducing Inflammatory and Oxidative Stress

doi: 10.3390/ijms23137004

Figure Lengend Snippet: CMP treatment reduces ARPE-19 inflammatory signaling: ELISA measurements. ( A ) Interleukin-6 (IL-6) secretion from ARPE-19 cells increased significantly following treatment with activated MMP-1 (60 nM) for 6 h compared to intact collagen control (#, p < 0.001). Following a complete exchange of media, cells were treated with 200 µM CMP 13A, which reduced Il-6 by 5-fold (*, p = 0.007) to control levels ( p = 0.99). Right: positive control using lipopolysaccharide (LPS, 10 mg/mL) shows +30-fold increase compared to control ( p <0.001). ( B ) Left: IL-6 secretion increased significantly following 24 h of 20 nM MMP-1 (#, p < 0.001). Concurrent treatment with CMP 13A significantly reduced Il-6 compared to MMP-1 ( p = 0.005), as did a combination of CMP 13A and 03A ( p = 0.014, concentration of each was 200 µM). Right: adding 200 µM CMP 13A at the 12 h mark for the remaining 12 h also reduced Il-6 compared to MMP-1 ( p = 0.001). ( C ) Interleukin-8 (IL-8) secretion from ARPE-19 cells also increased following MMP-1(6 h, 60 nM) compared to control (#, p < 0.001). Following complete media exchange, CMP 13A reduced Il-8 compared to both MMP-1 and control (*, p < 0.001). LPS positive control (right) induced a nearly 30-fold increase in IL-8 compared to control (#, p < 0.001). ( D ) IL-8 secretion did not change following 24 h of 20 nM MMP-1 alone or with concurrent treatment with CMP compared to control ( p = 0.30). For each measurement, n ≥ 6.

Article Snippet: Upon completion of the experiments, supernatants were collected and used to measure IL-6 (Human IL-6 ELISA Kit, Abcam, Waltham, MA, USA) and IL-8 (Human IL-8 ProQuantum, Thermo Fisher, Nashville, TN, USA), following the manufacturer’s instructions.

Techniques: Enzyme-linked Immunosorbent Assay, Positive Control, Concentration Assay