Fig. 6

Fucoidan inhibits FFA-induced inflammatory responses through the Nrf2 signaling pathway. (A-B) Fucoidan decreased the expression of inflammatory factors induced by FFAs in HepG2 cells. HepG2 cells were stimulated with FFAs (0.5 mM) for 24 h, further treatment with DMSO (control) or fucoidan (100 µg/ml) for additional 24 h. The expression of TNF-α and IL-6 were measured by qRT-PCR. (C) Fucoidan inhibited the phosphorylation of P65 NF-κB induced by FFAs in HepG2 cells. HepG2 cells were treated as described in (A-B), and the phosphorylation of P65 NF-κB were assayed by western blotting. (D-F) Fucoidan inhibited nuclear translocation of P65 NF-κB induced by FFAs in HepG2 cells. HepG2 cells were treated as described in (A-B), and the nuclear translocation of P65 NF-κB were assayed by western blotting and Immunofluorescence assay. (G-H) Nrf2 knock-down abolished the effect of fucoidan on the expression of inflammatory factors in spheroids. Spheroids with Nrf2 knocked down were stimulated with FFAs (0.5 mM) for 24 h, further treatment with DMSO (control) or fucoidan (100 µg/ml) for additional 24 h. The expression of TNF-α and IL-6 were measured by qRT-PCR. (I-K) Nrf2 knock-down inhibited the reduction of phosphorylation and nuclear translocation of P65 NF-κB by fucoidan in spheroids. Spheroids with Nrf2 knocked down were treated as described in (G-H), and the phosphorylation and nuclear translocation of P65 NF-κB were assayed by western blotting. Data were analyzed by student’s t test and expressed as the mean ± SD (n = 3). * represents the differences the two groups or compared to control group. ^# represents the differences compared to the DMSO group. ^a represents the differences compared to the FFA group. * P < 0.05; ** P < 0.01; ^#P < 0.05; ^##P < 0.01; ^aaP < 0.01