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AIM:To explore the protective effect and the relevant mechanisms of Fufang Biejia Ruangan Pills(FFBJRGP)on hepatic fibrosis in vivo and in vitro.METHODS:Hepatic fibrosis was induced by carbon tetrachloride composite factors.Adult Wistar rats were randomly divided into four groups:normal control group;hepatic fibrosis model group;FFBJRGP-treated group at a daily dose of 0.55 g/kg;and colchicinetreated group at a daily dose of 0.1 g/kg.The effects of FFBJRGP on liver function,serum levels of hyaluronic acid(HA),typeⅣcollagen(CⅣ),typeⅢprocollagen(PCⅢ),laminin(LN),histopathology,and expression of transforming growth factor(TGF-β1)and Smad3 in hepatic fibrosis were evaluated in vivo.The effects of FFBJRGP on survival rate,hydroxyproline content and cell cycle distribution were further detected in vitro.RESULTS:Compared with the hepatic fibrosis model group,rats treated with FFBJRGP showed a reduction in hepatic collagen deposition and improvement in hepatic lesions.Compared with those of the model group,the activities of alanine aminotransferase(62.0±23.7 U/L)and aspartate aminotransferase(98.8±40.0 U/L)in the FFBJRGP-treated group were decreased(50.02±3.7 U/L and 57.2±30.0 U/L,respectively,P<0.01).Compared with those in the model group,the levels of PCⅢ(35.73±17.90 g/mL),HA(563.82±335.54 ng/mL),LN(89.57±7.59 ng/mL)and CⅣ(29.20±6.17ng/mL)were decreased to 30.18±9.41,456.18±410.83,85.46±7.51 and 28.02±9.45 ng/mL,respectively.Reverse-transcriptase polymerase chain reaction and Western blotting also revealed that expression of TGF-β1 and Smad3 were down-regulated in vivo.Cell proliferation was inhibited,the level of hydroxyproline was decreased compared with the control group(P<0.01),and the cell cycle was redistributed when exposed to FFBJRGP in vitro.CONCLUSION:FFBJRGP inhibits hepatic fibrosis in vivo and in vitro,which is probably associated with downregulation of fibrogenic signal transduction of the TGF-β-Smad pathway.
AIM: To explore the protective effect and the relevant mechanisms of Fufang Biejia Ruangan Pills (FFBJRGP) on hepatic fibrosis in vivo and in vitro. METHODS: Hepatic fibrosis was induced by carbon tetrachloride composite factors. Adult Wistar rats were differentiated into four groups: normal control group; hepatic fibrosis model group; FFBJRGP-treated group at a daily dose of 0.55 g / kg; and colchicinetreated group at a daily dose of 0.1 g / kg. effects of FFBJRGP on liver function, serum levels of hyaluronic acid ( HA), type IV colagen (C IV), type III protocollagen (PC III), laminin (LN), histopathology, and expression of transforming growth factor (TGF-β1) and Smad3 in hepatic fibrosis were evaluated in vivo. content and cell cycle distribution were further detected in vitro .RESULTS: Compared with the hepatic fibrosis model group, rats treated with FFBJRGP showed a reduction in hepatic collagen deposition and improvement in hepatic lesions. Compared with th ose of the model group, the activities of alanine aminotransferase (62.0 ± 23.7 U / L) and aspartate aminotransferase (98.8 ± 40.0 U / L) in the FFBJRGP-treated group were decreased (50.02 ± 3.7 U / L and 57.2 ± 30.0 U /L,respectively,P<0.01).Compared with those in the model group, the levels of PCIII (35.73 ± 17.90 g / mL), HA (563.82 ± 335.54 ng / mL), LN (89.57 ± 7.59 ng / mL) and CⅣ (29.20 ± 6.17 ng / mL) were decreased to 30.18 ± 9.41,456.18 ± 410.83, 85.46 ± 7.51 and 28.02 ± 9.45 ng / mL respectively. Reverse-transcriptase polymerase chain reaction and Western blotting also revealed that expression of TGF- β1 and Smad3 were down-regulated in vivo. Cell proliferation was inhibit, the level of hydroxyproline was decreased compared with the control group (P <0.01), and the cell cycle was redistributed when exposed to FFBJRGP in vitro.CONCLUSION: FFBJRGP inhibits hepatic fibrosis in vivo and in vitro, which is probably associated with downregulation of fibrogenic signal transduction of the TGF-β-Smad pathway.