AIM: To investigate the effects of filtrate of fermented mycelia from Antrodia camphorata (FMAC) on liver fibrosis induced by carbon tetrachloride (CCl(4)) in rats. METHODS: Forty Wistar rats were divided randomly into control group and model group. All model rats were given 200 mL/L CCl(4) (2 mL/Kg, po) twice a week for 8 wk. Four weeks after CCl(4) treatment, thirty model rats were further divided randomly into 3 subgroups: CCl(4) and two FMAC subgroups. Rats in CCl(4) 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 beta1 (TGF-beta1) mRNA were detected by RT-PCR. Histochemical staining of Masson's trichrome was performed. RESULTS: CCl(4) caused liver fibrosis, featuring increased prothrombin time, hepatic MDA and HP contents, and spleen weight and decreased plasma albumin level. Compared with CCl(4) subgroup, FMAC subgroup (1 g/kg) significantly decreased the prothrombin time (36.7+/-7.2 and 25.1+/-10.2 in CCl(4) and FMAC groups, respectively, P<0.05) and increased plasma albumin concentration (22.7+/-1.0 and 30.7+/-2.5 in CCl(4) and FMAC groups, respectively, P<0.05). Spleen weight was significantly lower in rats treated with CCl(4) and FMAC (1 g/kg) compared to CCl(4) treated rats only (2.7+/-0.1 and 2.4+/-0.2 in CCl(4) and FMAC groups, respectively, P<0.05). The amounts of hepatic MDA and HP in CCl(4)+FAMC (1 g/kg) subgroup were also lower than those in CCl(4) subgroup (MDA: 3.9+/-0.1 and 2.4+/-0.6 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01; HP: 1730.7+/-258.0 and 1311.5+/-238.8 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01). Histologic examinations showed that CCl(4)+FMAC subgroups had thinner or less fibrotic septa than CCl(4) group. RT-PCR analysis indicated that FMAC (1 g/kg) reduced mRNA levels of collagen I, TIMP-1 and TGF-beta1 (collagen I: 5.63+/-2.08 and 1.78+/-0.48 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01; TIMP-1: 1.70+/-0.82 and 0.34+/-0.02 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01; TGF-beta1:38.03+/-11.9 and 4.26+/-2.17 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01) in the CCl(4)-treated liver. CONCLUSION: It demonstrates that FMAC can retard the progression of liver fibrosis induced by CCl(4) in rats.
AIM: To investigate the effects of filtrate of fermented mycelia from Antrodia camphorata (FMAC) on liver fibrosis induced by carbon tetrachloride (CCl(4)) in rats. METHODS: Forty Wistar rats were divided randomly into control group and model group. All model rats were given 200 mL/L CCl(4) (2 mL/Kg, po) twice a week for 8 wk. Four weeks after CCl(4) treatment, thirty model rats were further divided randomly into 3 subgroups: CCl(4) and two FMAC subgroups. Rats in CCl(4) 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 beta1 (TGF-beta1) mRNA were detected by RT-PCR. Histochemical staining of Masson's trichrome was performed. RESULTS:CCl(4) caused liver fibrosis, featuring increased prothrombin time, hepatic MDA and HP contents, and spleen weight and decreased plasma albumin level. Compared with CCl(4) subgroup, FMAC subgroup (1 g/kg) significantly decreased the prothrombin time (36.7+/-7.2 and 25.1+/-10.2 in CCl(4) and FMAC groups, respectively, P<0.05) and increased plasma albumin concentration (22.7+/-1.0 and 30.7+/-2.5 in CCl(4) and FMAC groups, respectively, P<0.05). Spleen weight was significantly lower in rats treated with CCl(4) and FMAC (1 g/kg) compared to CCl(4) treated rats only (2.7+/-0.1 and 2.4+/-0.2 in CCl(4) and FMAC groups, respectively, P<0.05). The amounts of hepatic MDA and HP in CCl(4)+FAMC (1 g/kg) subgroup were also lower than those in CCl(4) subgroup (MDA: 3.9+/-0.1 and 2.4+/-0.6 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01; HP: 1730.7+/-258.0 and 1311.5+/-238.8 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01). Histologic examinations showed that CCl(4)+FMAC subgroups had thinner or less fibrotic septa than CCl(4) group. RT-PCR analysis indicated that FMAC (1 g/kg) reduced mRNA levels of collagen I, TIMP-1 and TGF-beta1 (collagen I: 5.63+/-2.08 and 1.78+/-0.48 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01; TIMP-1: 1.70+/-0.82 and 0.34+/-0.02 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01; TGF-beta1:38.03+/-11.9 and 4.26+/-2.17 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01) in the CCl(4)-treated liver. CONCLUSION: It demonstrates that FMAC can retard the progression of liver fibrosis induced by CCl(4) in rats.