Fig. 5. Administration of cortistatin reversed the exacerbated cholestasis-induced liver fibrosis observed in cortistatin-deficient mice. (A ) Hepatic fibrosis was induced by bile duct ligation (BDL) in partially-deficient (CST+/- ) mice in cortistatin and treated i.p. with PBS or cortistatin as indicated in the diagram. (B ) Extension of hepatic fibrosis and necrosis were determined in Sirius red- and H&E-stained sections (7-10 mice/group). (C ) Presence of α-smooth muscle actin (αSMA)-positive myofibroblasts was quantified by immunofluorescence in liver sections (5-8 mice/group). (D ) Serum levels of direct bilirubin were measured 10d post-BDL (5-8 mice/group). (E ) Markers of hepatic fibrosis were determined by measuring collagen contents in liver protein extracts and gene expression of connective tissue growth factor (CTGF), αSMA and collagen1-α2 (Col1a2) in liver mRNA isolated 17 days post-BDL (8-10 mice/group). Scale bars: 100-µm. Data are the mean±SEM. *p<0.05, **p<0.01, ***p<0.001 vs. PBS-treated CST+/- mice, unpaired two-tailed Student’s t-test.