Skip to main content
. 2016 Oct 24;6:35855. doi: 10.1038/srep35855

Figure 5. Suppression of CCL22 expression by fucoidan is mediated by a p38- and PI3K-AKT- independent inhibition of the NF-κB pathway.

Figure 5

(a,b) THP-1-derived M2 macrophages were treated with the NF-κB inhibitor BAY11-7082, the PI3K inhibitor Wortmannin or the p38-MAPK inhibitor SB203580 for 24 h. The cells and culture supernatants were collected. CCL22 transcription (a) and concentration (b) were measured by quantitative real-time PCR and ELISA, respectively. (c) M2 macrophages derived from THP-1 cells were pretreated with the Wortmannin or the SB203580 for 30 min, followed by incubation with or without Fucoidan for 1 h. Whole-cell lysates were analyzed by western blot using the appropriate antibodies. The original blots are presented in Supplementary Fig. S2. Densitometry ratios of phospho-p65-NF-κB, AKT and p38-MAPK were normalized to β-actin levels. The cells treated with DMSO were used as control. The value represent means ± SD, n = 3. *P < 0.05, **P < 0.01 versus the control. (d) p65-NF-κB immunofluorescence of THP-1-derived M0 and M2 polarized macrophages, which were treated as described in (c). Green (anti-p65-NF-κB) indicates p65-NF-κB distribution, and blue indicates the location of nucleus. The scale bar represents 10 μm.