Fig. 7: Pharmacologic Kctd17 inhibition protects from MASH-induced liver fibrosis. | Experimental & Molecular Medicine

Fig. 7: Pharmacologic Kctd17 inhibition protects from MASH-induced liver fibrosis.

From: Hepatocyte KCTD17-mediated SERPINA3 inhibition determines liver fibrosis in metabolic dysfunction-associated steatohepatitis

Fig. 7

a C57BL/6 WT mice were fed FPC diet for 10 weeks and then administered control ASO or two different Kctd17-targeting ASO (Kctd17 ASO-1 and ASO-2) weekly by intraperitoneal injection a dose of 25 mg/kg and euthanized 6 weeks after the injections. b–e Liver Kctd17 mRNA levels (b) Serpina3k protein level in serum (c) liver gene expression (n = 6–7 per group) (d) H&E and Sirius red staining in histological sections of mouse liver, with respective quantification (n = 6 per group; scale bar, 100 μm; magnification, 20×) (e). f, g ALT (f) and AST (g) levels in serum. h C57BL/6 WT mice were fed CDAHFD for 6 weeks and then administered control ASO, Kctd17 ASO-1 or ASO-2 weekly by intraperitoneal injection a dose of 20 mg/kg and euthanized 6 weeks after the injections. i–l Liver Kctd17 mRNA levels (i), Serpina3k level in serum (j) liver gene expression (n = 7–8 per group) (k) and H&E and Sirius red staining in histological sections of mouse liver, with respective quantification (n = 4 per group; scale bar, 100 μm; magnification, 20×) (l). m, n ALT (m) and AST (n) levels in serum (n = 7 per group) in CDAHFD-fed control, Kctd17 ASO-1-treated or ASO-2-treated mice. *P < 0.05, **P < 0.01, ***P < 0.001 compared with that of the control ASO according to a two-way analysis of variance. All data are shown as the means ± s.e.m.

Back to article page