bay 11 7082 Search Results


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MedChemExpress nf κb pathway inhibitor bay 11 7082
Nf κb Pathway Inhibitor Bay 11 7082, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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InvivoGen bay117082
Bay117082, supplied by InvivoGen, 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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Santa Cruz Biotechnology nf κꞵ pathway
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Selleck Chemicals ex527
Figure 4. SIRT1 increased protein level of NF-κB p65 and its downstream targets upon metformin treatment in cancer cells. (a) SIRT1, PGC-1α, NF-κB p65, Bax, cytochrome c, cleaved-caspase3, GSDME-F and GSDME-N protein levels were detected in cells treated with 20 mM MET for 8 h in the absence or presence of 10 μM <t>EX527</t> for 24 h. (b) Protein levels of SIRT1, PGC-1α, NF-κB p65, cleaved- caspase3 and GSDME-N after MCF-7 cells were transfected with SIRT1 siRNA, incubated for 36 h and further treated with or without 20 mM MET for 8 h. *P < 0.05, **P < 0.01 compared with control.
Ex527, supplied by Selleck Chemicals, 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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Cell Signaling Technology Inc bay11 7082
Figure 4. SIRT1 increased protein level of NF-κB p65 and its downstream targets upon metformin treatment in cancer cells. (a) SIRT1, PGC-1α, NF-κB p65, Bax, cytochrome c, cleaved-caspase3, GSDME-F and GSDME-N protein levels were detected in cells treated with 20 mM MET for 8 h in the absence or presence of 10 μM <t>EX527</t> for 24 h. (b) Protein levels of SIRT1, PGC-1α, NF-κB p65, cleaved- caspase3 and GSDME-N after MCF-7 cells were transfected with SIRT1 siRNA, incubated for 36 h and further treated with or without 20 mM MET for 8 h. *P < 0.05, **P < 0.01 compared with control.
Bay11 7082, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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BPS Bioscience nsc 95397
Figure 4. SIRT1 increased protein level of NF-κB p65 and its downstream targets upon metformin treatment in cancer cells. (a) SIRT1, PGC-1α, NF-κB p65, Bax, cytochrome c, cleaved-caspase3, GSDME-F and GSDME-N protein levels were detected in cells treated with 20 mM MET for 8 h in the absence or presence of 10 μM <t>EX527</t> for 24 h. (b) Protein levels of SIRT1, PGC-1α, NF-κB p65, cleaved- caspase3 and GSDME-N after MCF-7 cells were transfected with SIRT1 siRNA, incubated for 36 h and further treated with or without 20 mM MET for 8 h. *P < 0.05, **P < 0.01 compared with control.
Nsc 95397, supplied by BPS Bioscience, 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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TargetMol nf κb inhibitor
<t>JAK-STAT,</t> NF-κB and p38 signaling pathways played important roles in SVCV-induced carp IL-10 production. EPC cells were infected or uninfected with SVCV at MOI of 0.5, followed by treatment with JAK inhibitor CP-690550 ( A , B ), STAT3 inhibitor STA-21 ( C , D ), NF-κB inhibitor <t>BAY11-7082</t> ( E , F ), p38 inhibitor SB202190 ( G , H ), JNK inhibitor SP600125 ( I , J ) or DMSO for 6 h, 12 h, 24 h and 48 h post-infection. The expression of carp IL-10 mRNA and protein were analyzed using RT-PCR and ELISA, respectively. Data are presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and, ns indicates no significant difference p > 0.05 compared with DMSO-treated plus SVCV-infected cells.
Nf κb Inhibitor, supplied by TargetMol, 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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BOC Sciences bay11 7082
PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or <t>BAY11-7082</t> (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6
Bay11 7082, supplied by BOC Sciences, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Sino Biological bay
PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or <t>BAY11-7082</t> (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6
Bay, supplied by Sino Biological, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Chem Impex International bay11 7082
PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or <t>BAY11-7082</t> (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6
Bay11 7082, supplied by Chem Impex International, 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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Sino Biological bay11 7082
PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or <t>BAY11-7082</t> (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6
Bay11 7082, supplied by Sino Biological, 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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Tokyo Chemical Industry bay 11-7082
PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or <t>BAY11-7082</t> (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6
Bay 11 7082, supplied by Tokyo Chemical Industry, 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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Image Search Results


Figure 4. SIRT1 increased protein level of NF-κB p65 and its downstream targets upon metformin treatment in cancer cells. (a) SIRT1, PGC-1α, NF-κB p65, Bax, cytochrome c, cleaved-caspase3, GSDME-F and GSDME-N protein levels were detected in cells treated with 20 mM MET for 8 h in the absence or presence of 10 μM EX527 for 24 h. (b) Protein levels of SIRT1, PGC-1α, NF-κB p65, cleaved- caspase3 and GSDME-N after MCF-7 cells were transfected with SIRT1 siRNA, incubated for 36 h and further treated with or without 20 mM MET for 8 h. *P < 0.05, **P < 0.01 compared with control.

Journal: Cell cycle (Georgetown, Tex.)

Article Title: Metformin activates AMPK/SIRT1/NF-κB pathway and induces mitochondrial dysfunction to drive caspase3/GSDME-mediated cancer cell pyroptosis.

doi: 10.1080/15384101.2020.1743911

Figure Lengend Snippet: Figure 4. SIRT1 increased protein level of NF-κB p65 and its downstream targets upon metformin treatment in cancer cells. (a) SIRT1, PGC-1α, NF-κB p65, Bax, cytochrome c, cleaved-caspase3, GSDME-F and GSDME-N protein levels were detected in cells treated with 20 mM MET for 8 h in the absence or presence of 10 μM EX527 for 24 h. (b) Protein levels of SIRT1, PGC-1α, NF-κB p65, cleaved- caspase3 and GSDME-N after MCF-7 cells were transfected with SIRT1 siRNA, incubated for 36 h and further treated with or without 20 mM MET for 8 h. *P < 0.05, **P < 0.01 compared with control.

Article Snippet: Cells were treated with 20 mM metformin (MET) (Sigma-Aldrich, St. Louis, USA) for diverse periods of time, 40 μM CCCP (Solarbio, Beijing, China) for 24 h, 10 μM EX527 (Selleck Chemicals, Houston, TX, USA) for 24 h, 10 μM BAY 11–7082 (Beyotime, Shanghai, China) for 1 h, and 3 μM Compound C (Selleck Chemicals, Houston, TX, USA) for 24 h supplemented with 10% FBS medium.

Techniques: Transfection, Incubation, Control

JAK-STAT, NF-κB and p38 signaling pathways played important roles in SVCV-induced carp IL-10 production. EPC cells were infected or uninfected with SVCV at MOI of 0.5, followed by treatment with JAK inhibitor CP-690550 ( A , B ), STAT3 inhibitor STA-21 ( C , D ), NF-κB inhibitor BAY11-7082 ( E , F ), p38 inhibitor SB202190 ( G , H ), JNK inhibitor SP600125 ( I , J ) or DMSO for 6 h, 12 h, 24 h and 48 h post-infection. The expression of carp IL-10 mRNA and protein were analyzed using RT-PCR and ELISA, respectively. Data are presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and, ns indicates no significant difference p > 0.05 compared with DMSO-treated plus SVCV-infected cells.

Journal: Microorganisms

Article Title: Spring Viremia of Carp Virus Infection Induces Carp IL-10 Expression, Both In Vitro and In Vivo

doi: 10.3390/microorganisms11112812

Figure Lengend Snippet: JAK-STAT, NF-κB and p38 signaling pathways played important roles in SVCV-induced carp IL-10 production. EPC cells were infected or uninfected with SVCV at MOI of 0.5, followed by treatment with JAK inhibitor CP-690550 ( A , B ), STAT3 inhibitor STA-21 ( C , D ), NF-κB inhibitor BAY11-7082 ( E , F ), p38 inhibitor SB202190 ( G , H ), JNK inhibitor SP600125 ( I , J ) or DMSO for 6 h, 12 h, 24 h and 48 h post-infection. The expression of carp IL-10 mRNA and protein were analyzed using RT-PCR and ELISA, respectively. Data are presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and, ns indicates no significant difference p > 0.05 compared with DMSO-treated plus SVCV-infected cells.

Article Snippet: JAK inhibitor (CP-690550), STAT3 inhibitor (STA-21), NF-κB inhibitor (BAY11-7082) and MAPK inhibitors (SP600125 and SB202190) were purchased from TargetMol (Shanghai, China).

Techniques: Infection, Expressing, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

( A – F ): Gene expressions of JAK1, JAK2, JAK3, TYK2, STAT5 and STAT6 were analyzed using RT-PCR in EPC cells. EPC cells were infected or uninfected with SVCV at MOI of 0.5, followed by treatment with CP-690550, STA-21, BAY11-7082, SB202190, SP600125 and DMSO, respectively, at 6 h, 12 h, 24 h and 48 h post-infection. The gene expressions were analyzed using RT-PCR. Data are presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 compared with DMSO-treated plus SVCV-infected cells.

Journal: Microorganisms

Article Title: Spring Viremia of Carp Virus Infection Induces Carp IL-10 Expression, Both In Vitro and In Vivo

doi: 10.3390/microorganisms11112812

Figure Lengend Snippet: ( A – F ): Gene expressions of JAK1, JAK2, JAK3, TYK2, STAT5 and STAT6 were analyzed using RT-PCR in EPC cells. EPC cells were infected or uninfected with SVCV at MOI of 0.5, followed by treatment with CP-690550, STA-21, BAY11-7082, SB202190, SP600125 and DMSO, respectively, at 6 h, 12 h, 24 h and 48 h post-infection. The gene expressions were analyzed using RT-PCR. Data are presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 compared with DMSO-treated plus SVCV-infected cells.

Article Snippet: JAK inhibitor (CP-690550), STAT3 inhibitor (STA-21), NF-κB inhibitor (BAY11-7082) and MAPK inhibitors (SP600125 and SB202190) were purchased from TargetMol (Shanghai, China).

Techniques: Reverse Transcription Polymerase Chain Reaction, Infection

PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or BAY11-7082 (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6

Journal: Respiratory Research

Article Title: Protectin conjugates in tissue regeneration 1 restores lipopolysaccharide-induced pulmonary endothelial glycocalyx loss via ALX/SIRT1/NF-kappa B axis

doi: 10.1186/s12931-021-01793-x

Figure Lengend Snippet: PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or BAY11-7082 (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6

Article Snippet: BAY11-7082 (NF-κB inhibitor, 20 mg/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or BOC-2(ALX receptor inhibitor, 600 ng/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. ( a, b ) The expression of HS in tissue was examined by immunofluorescence.

Techniques: Expressing, Western Blot, Injection

PCTR1 protects the endothelial glycocalyx by modulating SIRT1/NF-κB pathways via ALX receptor. The level of HPA, EXT-1, SIRT1 and p65 in lung tissues was quantified using western blotting assay. BAY11-7082 (NF-κB inhibitor, 20 mg/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or BOC-2(ALX receptor inhibitor, 600 ng/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. ( a, b ) The expression of HS in tissue was examined by immunofluorescence. HUVECs were administered with 1 µg/ml LPS and 100 nM PCTR1 for 6 h. After treatment with EX527 or DMSO, HS in HUVECs was determined by immunofluorescence ( c, d ). Scar bar = 50 μm. ** P < .01 in comparison to the CONTROL group, # P < .05, ## P < .01 in comparison to the LPS group, & P < .05, && P < .01, in comparison to the LPS + PCTR1 group. n = 6

Journal: Respiratory Research

Article Title: Protectin conjugates in tissue regeneration 1 restores lipopolysaccharide-induced pulmonary endothelial glycocalyx loss via ALX/SIRT1/NF-kappa B axis

doi: 10.1186/s12931-021-01793-x

Figure Lengend Snippet: PCTR1 protects the endothelial glycocalyx by modulating SIRT1/NF-κB pathways via ALX receptor. The level of HPA, EXT-1, SIRT1 and p65 in lung tissues was quantified using western blotting assay. BAY11-7082 (NF-κB inhibitor, 20 mg/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or BOC-2(ALX receptor inhibitor, 600 ng/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. ( a, b ) The expression of HS in tissue was examined by immunofluorescence. HUVECs were administered with 1 µg/ml LPS and 100 nM PCTR1 for 6 h. After treatment with EX527 or DMSO, HS in HUVECs was determined by immunofluorescence ( c, d ). Scar bar = 50 μm. ** P < .01 in comparison to the CONTROL group, # P < .05, ## P < .01 in comparison to the LPS group, & P < .05, && P < .01, in comparison to the LPS + PCTR1 group. n = 6

Article Snippet: BAY11-7082 (NF-κB inhibitor, 20 mg/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or BOC-2(ALX receptor inhibitor, 600 ng/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. ( a, b ) The expression of HS in tissue was examined by immunofluorescence.

Techniques: Western Blot, Injection, Expressing, Immunofluorescence