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

Figure 2 Zinc acetate and rifaximin on ethanol metabolism and accumulation of oxidative stress in alcoholic liver disease mice. A-C: Hepatic activity of alcohol dehydrogenase 1 (A), aldehyde dehydrogenase 2 (B) and cytochrome P450 2E1 (CYP2E1) (C). Quantitative values are indicated as fold changes to the values of C/V group; D-F: Hepatic levels of of catalase (D), superoxide dismutase (E) and malondialdehyde (F); G: Relative mRNA expression levels of Nox1, Nox2 and Nox4 in the liver of experimental mice. The mRNA expression levels were measured by RT-qPCR, and Gapdh was used as internal control. Quantitative values are indicated as fold changes to the values of C/V group. 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. ADH1: Alcohol dehydrogenase 1; ALDH2: Aldehyde dehydrogenase 2; CAT: Catalase; SOD: Superoxide dismutase; MDA: Malondialdehyde.