Fig. 5

Fucoidan alleviates FFA-induced lipid accumulation and oxidative stress via the Nrf2 signaling pathway. (A) Nrf2 knock-down inhibits the reduction in intracellular TG content by fucoidan in HepG2 cells. HepG2 cells 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. And then the intracellular TG content was measured. (B-F) Nrf2 knock-down inhibits the remission of oxidative stress by fucoidan in HepG2 cells. HepG2 cells with Nrf2 knocked down were treated as described in (A), and the intracellular levels of ROS, MDA, GSH, GR, and GPx were measured. (G) Nrf2 knock-down inhibits the reduction of intracellular TG content by fucoidan 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. And then the intracellular TG content was measured. (H-L) Nrf2 knock-down inhibits the remission of oxidative stress by fucoidan treatment in spheroids. Spheroids with Nrf2 knocked down were treated as described in (G), and the intracellular levels of ROS, MDA, GSH, GR, and GPx were measured. (M-O) Nrf2 knock-down inhibits the reduction of antioxidant factor expression by fucoidan in HepG2 cells. HepG2 cells with Nrf2 knocked down were treated as described in (A), and the expression of NQO1, GCLC, and HO-1 were assayed by western blotting. (P-R) Nrf2 knock-down inhibits the reduction of antioxidant factor expression by fucoidan in spheroids. Spheroids with Nrf2 knocked down were treated as described in (G), and the expression of NQO1, GCLC, and HO-1 were assayed by western blotting. Data were analyzed by student’s t test and expressed as the mean ± SD (n = 3). * represents the differences 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; ^aP < 0.05; ^aaP < 0.01