nf κb inhibitor jsh 23  (MedChemExpress)

Journal: Biology

Article Title: Shoseiryuto May Prevent Bronchial Epithelial Tight Junction Disruption by Inhibiting the Inflammatory NF-κB Signaling Pathway

doi: 10.3390/biology15080603

Figure Lengend Snippet: Cell viability of 16HBE cells treated with individual and combined concentrations of test agents. ( a ) SST, ( b ) ILQG, and GL derived from Glycyrrhiza , a component crude drug of SST, ( c ) NF-κB signaling inhibitors SC-514 and BAY-11-7085, ( d – g ) four proinflammatory agents ( d ) LPS, ( e ) H 2 O 2 ( f ) TNF-α, and ( g ) Poly I:C, and in combination with inflammatory inducers ( h ) 1 mg/mL LPS + SST, ( i ) 0.5 mM H 2 O 2 + SST, ( j ) 150 ng/mL TNF-α + SST, ( k ) 10 μg/mL Poly I:C + SST, ( l ) 10 μg/mL Poly I:C + ILQG or GL, and ( m ) 10 μg/mL Poly I:C + SC-514 or BAY-11-7085. Data are presented as mean ± SD ( n = 3). No significant differences were observed between the control (Ctrl) and treated groups (one-way ANOVA with Dunnett’s test).

Article Snippet: LPS and H 2 O 2 were sourced from Sigma-Aldrich (St. Louis, MO, USA); TNF-α from Fujifilm Wako (Osaka, Japan); Poly I:C from InvivoGen (San Diego, CA, USA); and the NF-κB inhibitors SC-514 and BAY11-7085 from Abcam (Cambridge, UK) and TargetMol (Boston, MA, USA), respectively.

Techniques: Derivative Assay, Control

Journal: Biology

Article Title: Shoseiryuto May Prevent Bronchial Epithelial Tight Junction Disruption by Inhibiting the Inflammatory NF-κB Signaling Pathway

doi: 10.3390/biology15080603

Figure Lengend Snippet: Effects of NF-κB signaling inhibitors SC-514 and BAY11-7085 on Poly I:C-induced inflammation and TJ barrier disruption. ( a , b ) Inflammatory markers: IL-6 medium concentration and IL-6 mRNA expression. ( c – f ) TJ barrier markers: TEER, Na–F permeability, occludin mRNA expression, and immunofluorescent-stained protein. Occludin is shown in red and nuclei are stained with DAPI (blue). Data are presented as mean ± SD ( n = 3). ** p < 0.01, *** p < 0.001 versus Ctrl; † p < 0.05, †† p < 0.01, ††† p < 0.001 versus Poly I:C (one-way ANOVA with Dunnett’s test).

Article Snippet: LPS and H 2 O 2 were sourced from Sigma-Aldrich (St. Louis, MO, USA); TNF-α from Fujifilm Wako (Osaka, Japan); Poly I:C from InvivoGen (San Diego, CA, USA); and the NF-κB inhibitors SC-514 and BAY11-7085 from Abcam (Cambridge, UK) and TargetMol (Boston, MA, USA), respectively.

Techniques: Disruption, Concentration Assay, Expressing, Permeability, Staining

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