Published online Apr 21, 2006. doi: 10.3748/wjg.v12.i15.2369
Revised: July 20, 2005
Accepted: December 22, 2005
Published online: April 21, 2006
AIM: To investigate the effects of filtrate of fermented mycelia from Antrodia camphorata (FMAC) on liver fibrosis induced by carbon tetrachloride (CCl4) in rats.
METHODS: Forty Wistar rats were divided randomly into control group and model group. All model rats were given 200 mL/L CCl4 (2 mL/Kg, po) twice a week for 8 wk. Four weeks after CCl4 treatment, thirty model rats were further divided randomly into 3 subgroups: CCl4 and two FMAC subgroups. Rats in CCl4 and 2 FMAC subgroups were treated with FMAC 0, 0.5 and 1.0 g/kg, daily via gastrogavage beginning at the fifth week and the end of the eighth week. Spleen weight, blood synthetic markers (albumin and prothrombin time) and hepatic malondialdehyde (MDA) and hydroxyproline (HP) concentrations were determined. Expression of collagen I, tissue inhibitor of metalloproteinases (TIMP)-1 and transforming growth factor β1 (TGF-β1) mRNA were detected by RT-PCR. Histochemical staining of Masson’s trichrome was performed.
RESULTS: CCl4 caused liver fibrosis, featuring increased prothrombin time, hepatic MDA and HP contents, and spleen weight and decreased plasma albumin level. Compared with CCl4 subgroup, FMAC subgroup (1 g/kg) significantly decreased the prothrombin time (36.7 ± 7.2 and 25.1 ± 10.2 in CCl4 and FMAC groups, respectively, P < 0.05) and increased plasma albumin concentration (22.7 ± 1.0 and 30.7 ± 2.5 in CCl4 and FMAC groups, respectively, P < 0.05). Spleen weight was significantly lower in rats treated with CCl4 and FMAC (1 g/kg) compared to CCl4 treated rats only (2.7 ± 0.1 and 2.4 ± 0.2 in CCl4 and FMAC groups, respectively, P < 0.05). The amounts of hepatic MDA and HP in CCl4 ± FAMC (1 g/kg) subgroup were also lower than those in CCl4 subgroup (MDA: 3.9 ± 0.1 and 2.4 ± 0.6 in CCl4 and CCl4 + FMAC groups, respectively, P < 0.01; HP: 1730.7 ± 258.0 and 1311.5 ± 238.8 in CCl4 and CCl4 + FMAC groups, respectively, P <0.01). Histologic examinations showed that CCl4 + FMAC subgroups had thinner or less fibrotic septa than CCl4 group. RT-PCR analysis indicated that FMAC (1 g/kg) reduced mRNA levels of collagen I, TIMP-1 and TGF-β1 (collagen I: 5.63 ± 2.08 and 1.78 ± 0.48 in CCl4 and CCl4 + FMAC groups, respectively, P < 0.01; TIMP-1: 1.70 ± 0.82 and 0.34 ± 0.02 in CCl4 and CCl4 + FMAC groups, respectively, P < 0.01; TGF-β1:38.03 ± 11.9 and 4.26 ± 2.17 in CCl4 and CCl4 + FMAC groups, respectively, P < 0.01) in the CCl4-treated liver.
CONCLUSION: It demonstrates that FMAC can retard the progression of liver fibrosis induced by CCl4 in rats.