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FilenameFormatSizeDescription
mnfr2130-sup-0001-FigureS1.tif5308KFigure S1. Effects of β-sitosterol on IKKβ phosphorylation, IkBα degradation, NF-κB activation in LPS-stimulated peritoneal macrophages Mouse peritoneal macrophages were treated with 50 ng/mL LPS in the absence or presence of β-sitosterol (10 or 20 μM). (A) Western blot analysis for TLR4, p-IRAK-1, IRAK-1, p-IKKβ, p-IkBα, p65, p-p65, COX2, INOS, and β-actin protein levels are shown. (B) NF-κB nuclear translocation was detected by confocal analysis using an antibody for the p65 subunit.
mnfr2130-sup-0002-FigureS2.tif753KFigure S2. Effects of β-sitosterol on IRAK phosphorylation and NF-κB activation in PGN-stimulated macrophages Mouse intestinal macrophages (A) or peritoneal macrophages (B) were treated with 50 ng/mL PGN in the absence or presence of β-sitosterol (10 or 20 μM). Western blot analysis for p-IRAK-1, IRAK-1, p65, p-p65, and β-actin protein levels are shown.
mnfr2130-sup-0003-FigureS3.jpg1299KFigure S3. Effects of β-sitosterol on the interaction between LPS and TLR4 in LPS-stimulated peritoneal macrophages (A) Effect on the binding of LPS on mouse peritoneal macrophages was measured by flow cytometry. Mouse peritoneal macrophages were incubated with Alexa Fluor 594-conjugated LPS (10 mg/mL) for 30 min in the absence or presence of β-Sitosterol. (B) Interaction between Alexa Flour 594-conjugated LPS and TLR4 was detected by confocal microscope analysis using an antibody for the TLR4 subunit. Mouse peritoneal macrophages were treated with 50 ng/mL LPS in the absence or presence of β-sitosterol (10 or 20 μM).

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