Fig. 1.

EA treatment attenuated hepatic injury and fibrosis induced by CCl₄ in mice

(A) The chemical structure of EA. (B) Body weights of mice receiving either control treatment or EA treatment with EA at doses of 25, 50 and 100 mg/kg body weight for 8 weeks (n = 40), and liver sections were subjected to H&E staining (n = 10). (C) Representative photographs show the pathological changes in the livers observed by macroscopic examination; liver sections were stained with H&E, Masson and Sirius Red. The liver fibrosis stage was scored in a double-blind method. The Masson and Sirius red staining areas of the mice and the liver/body weight ratio (D) were calculated. n = 10. (E) Liver function was assessed by ALT, AST and LDH activities, and (F) three items of liver fiber (PC-III, LN and collagen) in the serum of mice were measured by commercial kits or ELISA kits. n = 10. (G) Western blot and (H) qPCR assays were used to detect the protein and mRNA expression levels of α-SMA, Col1a1, TGF-β1 and desmin in isolated primary HSCs from liver tissue and quantify them. n = 5. (I) Collagen content was measured by biochemical determination of hydroxyproline (per mg of liver) in the livers of mice. n = 10. (J) Immunohistochemical staining of α-SMA and TGF-β1 was determined in liver sections. Brown arrow indicates positive area. n = 5. Data are expressed as the mean ± SEM of three independent experiments; *P < 0.05, **P < 0.01 between the indicated groups. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)