Fig. 2.

EA treatment suppresses BDL-induced liver fibrosis and inhibits the activation of HSCs

(A) Representative images of liver sections from control and BDL mice treated with or without EA are shown. Liver sections (4 μm) were stained with H&E and Sirius Red for histopathological study and IHC for α-SMA or TGF-β1 were performed on the liver sections of mice. The Sirius Red, α-SMA and TGF-β1 staining areas of the mice were calculated. n = 10. (B) Western blot and (C) qPCR assays were used to detect the protein and mRNA expression levels of α-SMA and TGF-β1 in isolated primary HSCs from liver tissue and quantify them. n = 5. (D) Liver hydroxyproline levels were determined using a hydroxyproline assay kit in mice. n = 10. (E) Western blot and (F) qPCR assays were used to detect the protein and mRNA expression levels of α-SMA, Col1a1 and desmin in primary HSCs and LX-2 cells treated with TGF-β1 or/with EA and quantify them. n = 5. (G) qPCR assays were used to detect the mRNA expression levels of Mmp-2 and Mmp-9 in cells as described above. n = 5. (H) The inhibition ratio of cell growth was calculated in primary HSCs and LX-2 cells treated with EA and the apoptosis inhibitor ZVAD-FMK for 24 h n = 5. Data are expressed as the mean ± SEM of three independent experiments; *P < 0.05, **P < 0.01 between the indicated groups. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)