Fig. 1

GSTA3 levels were decreased in DMN- and CCL₄-induced rat liver fibrosis, and AKF-PD restored GSTA3 expression. a DMN and CCL₄ induced fibrosis in the rat liver. Representative photographs from each experimental group are shown (n = 10). Scale bar = 200 µm. b Schematic depicting the induction of experimental hepatic fibrosis by DMN or CCl₄ in rats and the administration of AKF-PD by oral gavage. Hepatic fibrosis was induced by intraperitoneal injections of 10 μl of DMN (diluted 1:100 with 0.15 M NaCl) per kg of body weight or 2 ml of CCl₄ (diluted 1:1 in olive oil) per kg of body weight. c RT-PCR analysis of the hepatic levels of the GSTA3 mRNA (n = 3). d WB analysis of the hepatic levels of the GSTA3, α-SMA and FN proteins. GAPDH levels were analyzed as a loading control (n = 3). e Immunohistochemical staining for 4-HNE in rat liver sections. (n = 5). Scale bar = 100 µm. f ELISA of MDA levels in rat serum (n = 3). Values are presented as mean ± SD. *P < 0.05 compared with the control group and ^#P < 0.05 compared with the DMN or CCl₄ group. GSTA3, glutathione S-transferase A3; DMN, dimethylnitrosamine; CCl₄, carbon tetrachloride; AKF-PD, fluorofenidone; α-SMA, α-smooth muscle actin; FN, fibronectin; GAPDH,; 4-HNE, 4-hydroxynonenal; MDA, malondialdehyde