nf κb inhibitor bay11 7082  (MedChemExpress)

Journal: Journal of Molecular Histology

Article Title: Interleukin-1 Receptor-Associated Kinase 3 Attenuates Chondrocyte Senescence and Osteoarthritis via Inhibition of the TLR7/9–NF-κB Axis

doi: 10.1007/s10735-026-10804-4

Figure Lengend Snippet: illustrates how IRAK3 inhibits NF-κB, thereby reducing inflammation and aging in chondrocytes. BAY 11-7082 is an IκBα phosphorylation and NF-κB inhibitor. The treatment concentration is 2 µM and the treatment time is 48 h. It was purchased from MedChemExpress, HY-13,453. Panel A shows the results of Western blotting, which was employed to assess the expression levels of p65 and phosphorylated p65 (p-p65) following the knockdown of IRAK3. Panel B presents the intensity and localization of p-65 as determined by immunofluorescence staining. Panels C through E display ELISA results for the detection of IL-1β, IL-6, and TNF-α expressions. Panel F shows β-galactosidase staining used to identify senescent chondrocytes. Panel G quantifies the number of positive cells. Statistical significance is indicated as follows: * p < 0.05, *** p < 0.001

Article Snippet: The NF-κB inhibitor BAY 11-7082, along with TLR7/9 agonists and inhibitors, were procured from MedChemExpress.

Techniques: Phospho-proteomics, Concentration Assay, Western Blot, Expressing, Knockdown, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: HCV infection induces dysregulation of glucose-stimulated insulin secretion via the TLR3/TRIF/NF-κB-iNOS-NO axis: Implications for prediabetes in HCV patients

doi: 10.1007/s00018-025-06072-2

Figure Lengend Snippet: HCV infection activated the NF-κB signaling pathway in β cells. ( A ) MIN6 cells were mock-infected or infected with 1.0 MOI of purified HCV. The presence of HCV positive strands and negative strands was detected in situ using molecular beacon probes (green). Double-stranded RNA (dsRNA) was identified via immunofluorescence assay using the J2 antibody (green). Nuclei were stained with DAPI (blue fluorescence), as shown. Scale bars, 10 μm. ( B ) MIN6 cells were transfected with the NF-κB luciferase reporter plasmid ( n = 3 biological experiments). Twenty-four hours after transfection, the NF-κB luciferase activity was quantitatively assessed at various time points following HCV infection. ( C ) Confocal microscopy images of MIN6 cells, either uninfected (first row) or infected for 24 h or 48 h at 1.0 MOI with HCV, probed with DAPI (blue) and anti-p65 (green). Scale bar, 10 μm. ( D ) Immunoblot analysis of p65 phosphorylation at Ser536, respectively, total p65 and Actin in MIN6 cells, either uninfected or infected with HCV. Values represent mean ± SD. *, p < 0.05; ***, p < 0.001

Article Snippet: The NF-κB inhibitors BAY 11–7082 and Pyrrolidinedithiocarbamate ammonium (PDTC) were obtained from MCE (MedChemExpress, USA).

Techniques: Infection, Purification, In Situ, Immunofluorescence, Staining, Fluorescence, Transfection, Luciferase, Plasmid Preparation, Activity Assay, Confocal Microscopy, Western Blot, Phospho-proteomics

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: HCV infection induces dysregulation of glucose-stimulated insulin secretion via the TLR3/TRIF/NF-κB-iNOS-NO axis: Implications for prediabetes in HCV patients

doi: 10.1007/s00018-025-06072-2

Figure Lengend Snippet: HCV stimulated the expression of iNOS via TLR3/Trif/NF-κB pathway. ( A ) DAF-FM DA measurements were detected following HCV infection in the presence of NF-κB inhibitor, BAY 11–7082 (100 μM). The NOS inhibitors L-NMMA (total NOS inhibitor, 100 μM) and 1400 W (iNOS inhibitor, 100 μM) were used as the positive control ( n = 6 biological experiments). ( B ) Immunoblot analysis of phosphorylated ( p -) or total p65, iNOS or Actin (loading control throughout) in MIN6 cells. The cells were infected with HCV for 12 h and subsequently treated with BAY or L-NMMA or left untreated. ( C ) Islets were isolated from C57BL/6N mice or from Tlr3 −/− , Tlr4 −/− , Tlr7 −/− , Tlr7/Tlr9 −/− or Trif/Myd88 . −/− knockout single or double knockout mice and then infected with HCV for 24 h. Insulin secretion were measured under low glucose conditions (3.3 mM) in the presence of BAY (100 μM) or PDTC (100 μM) ( n = 3 biological experiments). ( D ) Immunoblot analysis was conducted to evaluate the levels of p-p65 or total p65, as well as iNOS or Actin, in islets isolated from the indicated mice. ( E ) Insulin secretion was measured in islets derived from the indicated mice following 24-h HCV infection ( n = 3 biological experiments). Values represent mean ± SD. *, p < 0.05; **, p < 0.01; ***, p < 0.001

Article Snippet: The NF-κB inhibitors BAY 11–7082 and Pyrrolidinedithiocarbamate ammonium (PDTC) were obtained from MCE (MedChemExpress, USA).

Techniques: Expressing, Infection, Positive Control, Western Blot, Control, Isolation, Knock-Out, Double Knockout, Derivative Assay