Skip to main content
Fig. 1 | Nutrition & Metabolism

Fig. 1

From: Dihydromyricetin ameliorates liver fibrosis via inhibition of hepatic stellate cells by inducing autophagy and natural killer cell-mediated killing effect

Fig. 1

DHM administration ameliorated CCl4-induced liver fibrosis and HSCs activation in vivo. a Body weight was recorded. b–c Serum levels of aspartate transaminase ALT and AST. d Liver fibrosis was examined by H&E and Sirius Red stainings. e–g The mRNA expressions of CoL-1α1 (e), CoL-1α2 (f) and TIMP-1 (g) were detected by qRT-PCR. h The protein levels of MMP1, desmin, and α-SMA were analyzed by western blot. i–k The quantification of MMP-1 (i), desmin (j), and α-SMA (k) were displayed by histogram, respectively. Data were presented as mean ± SEM (n = 3); l HSCs activation was visualized by immunofluorescence assay of α-SMA. m The quantification of α-SMA by immunofluorescence assay were displayed by histogram. Data were presented as mean ± SEM (n = 3); *p < 0.05, **p < 0.01, compared to the control group; #p < 0.05, ##p < 0.01, compared to the CCl4 group. ALT, alanine transaminaseT; AST, aspartate transaminase; α-SMA, α-smooth muscle actin; CCl4, carbon tetrachloride; CoL-1α1, collagen I alpha 1; CoL-1α2, collagen I alpha 2; DHM, dihydromyricetin; H&E, hematoxylin and eosin; HSCs, hepatic stellate cells; MMP-1, metalloproteinase 1; TIMP-1, tissue inhibitor of metalloproteinases 1; qRT-PCR, quantitative real-time polymerase chain reaction

Back to article page