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. Author manuscript; available in PMC: 2016 Nov 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2015 Oct 1;35(11):2391–2400. doi: 10.1161/ATVBAHA.115.306474

Figure 4. Dose dependent effect of exogenous cFN on TLR4-mediated inflammation in macrophages.

Figure 4

Pooled bone marrow-derived macrophages from EDA−/−Apoe−/− and EDA−/−TLR4−/−Apoe−/− mice (n=4-5 mice/group) were stimulated in presence of cFN (0-50 μg/mL) for 24 hours. A. Top panel shows representative immunoblots showing expression of phosphorylated- NFkB p65, total NFkB p65 and β-actin. Bar diagram in middle and bottom panels represent quantification of intensity of phosphorylated- NFkB p65 to total NFkB p65 and phosphorylated- NFkB p65 to β-actin (loading control). N = 3 experiments/group. B&C. ELISA quantification of TNF-α and IL-1β in supernatant medium from cFN treated and untreated macrophages. Data is presented as mean ± SEM. N = 3 experiments/group.

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