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. 2014 Aug 25;35(10):1274–1284. doi: 10.1038/aps.2014.70

Figure 3.

Figure 3

Arctigenin regulated antioxidant-related pathways depending on AMPK activation. (A, B) Differentiated L6 cells were incubated with or without 10 μmol/L compound C (AMPK inhibitor) for 1 h before and during the incubation with arctigenin (20 μmol/L) for 2 h. After harvesting, total- and phospho-p53 protein levels (A), and Nrf2 in the cell nucleus and cytoplasm (B) were analyzed by Western blotting. (C) Differentiated L6 cells were incubated with 30 μmol/L PFT and arctigenin (20 μmol/L) for 2 h. After harvested, the amount of Nrf2 in the cell nucleus and cytoplasm were analyzed by Western blotting. (D) Differentiated L6 cells were treated with or without 10 μmol/L compound C (AMPK inhibitor) for 1 h before and during the incubation with arctigenin (20 μmol/L) for 24 h. The expression levels of Cu,Zn-SOD, Txn, Gsr, GPX1, UCP2, p21, PPARα and PGC-1α were measured by qRT-PCR. GAPDH RNA was used as an internal control for calculating mRNA fold changes. (E) Differentiated L6 cells were incubated with 30 μmol/L PFT and arctigenin (20 μmol/L) for 24 h. The expression levels of Cu,Zn-SOD, Txn, Gsr, GPX1, and p21 were measured by qRT-PCR. GAPDH RNA was used as an internal control for calculating mRNA fold changes. The results shown were validated by three independent experiments. Values are expressed as the mean±SEM. bP<0.05, cP<0.01. one-way ANOVA.