Fig. 6.

PPARα upregulation is required for curcumin to induce autophagy activation and inhibit hepatocyte epithelial-mesenchymal transition. PPAR-α activity of BNL CL.2 inhibited by GW6471 treatment. And cells were induced with TGF-β (2 ng·mL⁻¹) or interfered with curcumin (20 μM/L). A–B: Western blot and Real-time PCR analysis were used to detect the expression of PPARα, AMPK, mTOR, SQSTM1, α-SMA, Vimentin and LC3 (x ± s, n ≥ 3). β-Actin was used as an invariant control for equal loading. GAPDH was used as an invariant control for equal loading. ROS and GSH were tested with the corresponding kit. Compared with the control group ^#P < 0.05, ^##P < 0.01,^###P < 0.001; Compared with the model group (TGF-β, 2 ng·mL⁻¹) *P < 0.05, **P < 0.01; Compared with the TGF plus curcumin group ^$P < 0.05,^$$P < 0.01.