Dual therapy with vildagliptin and sacubitril/valsartan alleviates portal hypertension and inhibits soluble epoxide hydrolase in cirrhotic rats

Figure 7 Portal pressure, sinusoidal capillarization and hepatic fibrosis in bile duct-ligated rats. A: Experimental design of bile duct-ligated rats; B and C: Portal vein pressure (B) and portal blood flow (C) at the end of experiment; D: Immunofluorescence with cluster of differentiation 34, hematoxylin and eosin and Sirius-red staining in liver tissues; E: Quantification of cluster of differentiation 34-positive sinusoidal capillarization; F: Quantification of Sirius-red-stained fibrotic area; G: Hepatic message RNA (mRNA) levels of Acta2 and Col1a1. The mRNA expression levels were measured by quantitative real-time polymerase chain reaction, and glyceraldehyde-3-phosphate dehydrogenase was used as internal control. Quantitative values are indicated as fold changes to the values of sham-operated group + vehicle (saline)-treated group (E) or bile duct-ligated groups + vehicle (saline)-treated group (F and G). Data are the mean ± SD (n = 4, B, C and E-G). ^aP < 0.05; ^bP < 0.01. Significant difference between groups determined by Mann-Whitney U test. BDL: Bile duct-ligated; mRNA: Message RNA; DAPI: 4’,6-diamidino-2-phenylindole; CD34: Cluster of differentiation 34; HE: Hematoxylin and eosin; Sham: Sham-operated group; Veh: Vehicle (saline)-treated groups; DP4i: Dipeptidyl peptidase-4 inhibitor (vildagliptin)-treated group; ARNI group: Angiotensin receptor-neprilysin inhibitor (sacubitril/valsartan)-treated group; “Both group” defined dipeptidyl peptidase-4 inhibitor and angiotensin receptor-neprilysin inhibitor-treated group.