Fig 2: Preparation of the PC-DCN liposome, (a) Schematic illustration of the preparation of PC-DCN liposomes. (b) Characterization of liposomes by schematic diagram. (c) The average particle size of PC-DCN was represented by a histogram.

Fig 3: PC-DCN reduced cell proliferation in HSC-T6 cells by inhibiting fibrosis-related protein expression. (a) EdU assay for determining cell proliferation following treatment with PC-DCN. ***P < 0.001 vs. control. (b) Oil Red O staining was performed to analyze the lipid status in different groups. (c) Western blotting was used to detect the expression of fibrosis-related proteins (a-SMA, COL1A1), TGF-ß, and DCN after treatment with or without PC-DCN. ***P < 0.001 vs. control. (d) The a-SMA expression after treatment with PC-DCN was examined by immunofluorescence analysis.

Fig 4: (a) Western Blot analysis of a-SMA, COL1A1, TGF-ß, and DCN protein expression following PC-DCN intravenous or bile duct administration under CCl4 induction in mice. ***P < 0.001 vs. control; ###P < 0.001 vs. CCl4. (b) H&E staining showing the expression of a-SMA and TGF-ß following PC-DCN intravenous or bile duct administration under CCl4 induction in mice. ***P < 0.001 vs. control; ###P < 0.001 vs. CCl4.

Fig 5: Antifibrotic effect of PC-DCN in vivo. (a) The histopathology of liver tissue in different treatment groups (control, CCl4) stained using H&E. (b) Masson staining showed the changes in liver collagen fibers. (c–e) The levels of ASL, ALT, and TBIL under different treatment regimens were detected by ELISA. ***P < 0.001 vs. control; ###P < 0.001 vs. CCl4. (f) Real-time PCR confirmed proinflammatory cytokines IL-6, TNF-a, and IL-1ß expression after treatment with PC-DCN.