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AIM: To investigate the effects of filtrate of fermented mycelia from Antrodia camphorata (FMAC) on liver fibro-sis induced by carbon tetrachloride (CCI4) in rats. METHODS: Forty Wistar rats were divided randomly into control group and model group. All model rats were given 200 mL/L CCI4 (2 mL/Kg, po) twice a week for 8 wk. Four weeks after CCI4 treatment, thirty model rats were further divided randomly into 3 subgroups: CCI4 and two FMAC subgroups. Rats in CCI4 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 malondial-dehyde (MDA) and hydroxyproline (HP) concentrations were determined. Expression of collagen I, tissue inhibitor of metalloproteinases (TIMP)-1 and transforming growth factorβ1 (TGF-β1) mRNA were detected by RT-PCR. Histochemical staining of Masson’s trichrome was performed. RESULTS: CCI4 caused liver fibrosis, featuring increased prothrombin time, hepatic MDA and HP contents, and spleen weight and decreased plasma albumin level. Compared with CCI4 subgroup, FMAC subgroup (1 g/kg) significantly decreased the prothrombin time (36.7±7.2 and 25.1±10.2 in CCI4 and FMAC groups, respectively, P<0.05) and increased plasma albumin concentration (22.7±1.0 and 30.7±2.5 in CCI4 and FMAC groups, respectively, P< 0.05). Spleen weight was significantly lower in rats treated with CCI4 and FMAC (1 g/kg) compared to CCI4 treated rats only (2.7±0.1 and 2.4±0.2 in CCI4 and FMAC groups, respectively, P<0.05). The amounts of hepatic MDA and HP in CCI4±FAMC (1 g/kg) subgroup were also lower than those in CCI4 subgroup (MDA: 3.9±0.1 and 2.4±0.6 in CCI4 and CCI4 + FMAC groups, respectively, P< 0.01; HP: 1730.7±258.0 and 1311.5±238.8 in CCI4 and CCI4 + FMAC groups, respectively, P<0.01). Histologic examinations showed that CCI4 + FMAC subgroups had thinner or less fibrotic septa than CCI4 group. RT-PCR analysis indicated that FMAC (1 g/kg) reduced mRNA levels of collagen I, TIMP-1 and TGF-β1 (collagenⅠ: 5.63±2.08 and 1.78±0.48 in CCI4 and CCI4 + FMAC groups, respectively, P<0.01; TIMP-1: 1.70±0.82 and 0.34±0.02 in CCI4 and CCI4 + FMAC groups, respectively, P<0.01; TGF-β1:38.03±11.9 and 4.26±2.17 in CCI4 and CCI4+FMAC groups, respectively, P<0.01) in the CCI4-treated liver. CONCLUSION: It demonstrates that FMAC can retard the progression of liver fibrosis induced by CCI4 in rats.
AIM: To investigate the effects of filtrate of fermented mycelia from Antrodia camphorata (FMAC) on liver fibro-sis induced by carbon tetrachloride (CCI4) in rats. METHODS: Forty Wistar rats were divided into control group and model group. All model rats Four weeks after CCI4 treatment, thirty model rats were further divided into 3 subgroups: CCI4 and two FMAC subgroups. Rats in CCI4 and 2 (2 mL / Kg, po) twice a week for 8 weeks 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 malondial-dehyde 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 : CCI4 ca Compared with CCI4 subgroup, FMAC subgroup (1 g / kg) significantly decreased the prothrombin time (36.7 ± 7.2 and 25.1 ± 10.2 in CCI4 and FMAC groups, respectively, P <0.05) and increased plasma albumin concentration (22.7 ± 1.0 and 30.7 ± 2.5 in CCI4 and FMAC groups, respectively, P <0.05). Spleen weight was significantly lower in rats treated with CCI4 and FMAC (1 g / kg) compared to CCI4 treated rats (2.7 ± 0.1 and 2.4 ± 0.2 in CCI4 and FMAC groups, respectively, P <0.05). The amounts of hepatic MDA and HP in CCI4 ± FAMC (1 g / kg) subgroup were also lower than those in CCI4 subgroup (MDA: 3.9 ± 0.1 and 2.4 ± 0.6 in CCI4 and CCI4 + FMAC groups, respectively, P <0.01; HP: 1730.7 ± 258.0 and 1311.5 ± 238.8 in CCI4 and CCI4 + FMAC groups, respectively, P <0.01). Histologic examinations showed that CCI4 + FMAC subgroups had thinner or less fibrotic septa than C CI4 group. RT-PCR analysis indicated that FMAC (1 g / kg) reduced mRNA levels of collagen I, TIMP-1 and TGF-β1 (collagenⅠ: 5.63 ± 2.08 and 1.78 ± 0.48 in CCI4 and CCI4 + FMAC groups, respectively, P <0.01; TIMP-1: 1.70 ± 0.82 and 0.34 ± 0.02 in CCI4 and CCI4 + FMAC groups, respectively, P <0.01; TGF-β1: 38.03 ± 11.9 and 4.26 ± 2.17 in CCI4 and CCI4 + FMAC groups, respectively, in the CCI4-treated liver. CONCLUSION: It demonstrates that FMAC can retard the progression of liver fibrosis induced by CCI4 in rats.