Serelaxin increases the antifibrotic action of rosiglitazone in a model of hepatic fibrosis

Figure 1 Total liver collagen content. A: Sirius red staining of liver tissue from control (Con), fibrotic (CCl₄), rosiglitazone (Rosi), serelaxin (Rln) or combination-treated (Rosi + Rln) mice. Bar: 100 μm. B: Sirius red staining quantified. Data are expressed as mean ± SE, and analyzed by ANOVA (n = 5). ^aP < 0.001 vs Con; ^bP < 0.05 vs CCl₄, Rosi, or Rln.

Figure 2 Liver type I collagen content. A: Immunohistochemical staining of liver tissue from control (Con), fibrotic (CCl₄), rosiglitazone (Rosi), serelaxin (Rln) or combination-treated (Rosi + Rln) mice. Bar: 100 μm; B: Type I collagen staining quantified; C: Type I collagen gene expression determined by qPCR. Data are expressed as mean ± SE, and analyzed by ANOVA (n = 5). ^aP < 0.05 vs Con; ^bP < 0.05 vs CCl₄, Rosi, or Rln.

Figure 3 Liver smooth muscle actin content. A: Immunohistochemistry of liver tissue for SMA content from control (Con), fibrotic (CCl₄), rosiglitazone (Rosi), serelaxin (Rln) or combination-treated (Rosi+Rln) mice. Bar: 100 μm; B: SMA staining quantified. Data are expressed as mean ± SE, and analyzed by ANOVA (n = 5). ^aP < 0.001 vs Con; ^bP < 0.05 vs CCl₄; ^cP < 0.05 vs CCl₄, Rosi, or Rln.

Figure 4 Western blotting of PGC1α content in livers from control (Con), fibrotic (CCl₄), rosiglitazone (Rosi), serelaxin (Rln) or combination-treated (Rosi + Rln) mice. A: Liver tissue extracts were analyzed by Western blotting for PGC1α. The levels of GAPDH are shown as a loading control; B: The levels of PGC1α relative to GAPDH were determined by densitometry. Data are shown as mean Data are expressed as mean ± SE, and analyzed by ANOVA (n = 5). ^aP < 0.05 vs Con; ^bP < 0.01 vs CCl₄ or Rosi.