Dual therapy with zinc acetate and rifaximin prevents from ethanol-induced liver fibrosis by maintaining intestinal barrier integrity

Figure 1 Zinc acetate and rifaximin against hepatic steatosis in alcoholic liver disease mice. A: Experimental protocols; B: Changes in body weights during experimental period; C: Ratio of liver weight to body weight at the end of experiment; D: Zinc concentrations of the serum (left) and the liver (right); E: Serum levels of aspartate aminotransferase (left) and alanine aminotransferase (right); F: Representative macroscopic appearances (upper), microphotographs of hematoxylin and eosin (middle) and Oil Red O staining (lower) of the livers in the experimental mice. Scale bar: 25 μm; G: Semi-quantification of lipid accumulation stained by Oil Red O in high-power field by NIH imageJ software. Histochemical quantitative analyses included five fields per section. Quantitative values are indicated as fold changes to the values of C/V group; H: Hepatic concentrations of triglyceride. Data are mean ± SD (n = 10), ^aP < 0.05 and ^bP < 0.01 vs C/V group; ^cP < 0.05 and ^dP < 0.01 vs E/V group; ^eP < 0.05 and ^fP < 0.01 vs E/Zn group; ^gP < 0.05 and ^hP < 0.01 vs E/RFX group. AST: Aspartate aminotransferase; ALT: Alanine aminotransferase; HE: Hematoxylin and eosin.