Fig. 1.

Curcumin inhibits hepatic fibrosis and epithelial-mesenchymal transition and activates autophagy in vivo. Rats were divided into five groups: control group (no CCl₄, untreated); model group (CCl₄ injection, no treatment); Curcumin (100 mg/kg) and CCl₄ treatment group; Curcumin (200 mg/kg) and CCl₄ treatment group; Curcumin (400 mg/kg) and CCl₄ treatment group. A: Hepatic general examination of hematoxylin-eosin (HE), Masson and Sirius red stained (200 × ). B: Levels of serum alanine aminotransfease (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), lactic dehydrogenase (LDH), hydroxyproline (HYP), hyaluronic acid (HA), procollagen III (PC III) and Collagen IV. C: Immunofluorescence analysis of α-SMA and LC3 in fibrotic liver (200 × ). D: Immunofluorescence analysis of Vimentin and LC3 in fibrotic liver (200 × ). E: Protein expression of α-SMA, Vimentin, ATG-7, Beclin-1 and MAP-LC3 (x ± s, n ≥ 3). β-Actin was used as an invariant control for equal loading. Compared with the control group ^###P < 0.001; Compared with the model group *P < 0.05, **P < 0.01, ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)