Fig. 2

DHM treatment inhibited TGF-β1-induced HSCs activation in vitro. a Cell viability of LX2 treated by TGF-β1 was detected by CCK-8. b The level of collagen I in the cell supernatant was detected by ELISA kit. c–e After pretreated with DHM for 2 h and followed by TGF-β1 (5 ng/ml) treatment for 24 h, the cell viability of LX2 was determined by CCK-8 assay (c), and the levels of collagen I (d) and α-SMA (e) in cell supernatant were detected by the corresponding ELISA kit. f–g Representative images of collagen I immunofluorescence staining in LX2 cells. Green fluorescence represents the expression of collagen I and blue fluorescence with DAPI (staining represent cell nucleus) (f). The bar charts show the quantification of fluorescence intensity of collagen I (g). h–i Representative images of α-SMA immunofluorescence staining in LX2 cells. Green fluorescence represents the expression of α-SMA and blue fluorescence with DAPI staining represents cell nucleus (h). The bar charts show quantification of fluorescence intensity of α-SMA (i). Data were presented as mean ± SEM (n = 3); *p < 0.05, **p < 0.01, compared to the control group; ^##p < 0.01, compared to TGF-β1 group. CCK-8, Cell Counting Kit-8; DAPI, 4′,6-diamidino-2-phenylindole; ELISA, enzyme-linked immunosorbent assay; TGF-β1, transforming growth factor-beta 1