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Objeclive:To investigate the effect of Ganfukang(肝复康,GFK)on connective tissue growth factor(CTGF)and focal adhesion Kinase(FAK)/protein kinase B(PKB or Akt)signal pathway in a hepatic fibrosis rat model and to explore the underlying therapeutic molecular mechanisms of GFK.Methods:Fifty SD rats were randomly divided into five groups as follows:the control group,the model group(repeated subcutaneous injection of CCl_4),and the three GFK treatment groups(31.25,312.5,and 3125 mg/kg,intragastric administration).Reverse transcriptase-polymerase chain reaction(RT-PCR),Western blotting,and immunohistochemistry were used to examine the expression of CTGF,integrin α5,integrin β1,FAK/Akt signal pathway,cyclinD1,and collagen in the different-treated rats.Results:GFK attenuated the up-regulation of CTGF,integrin α5,and integrin β1 in hepatic fibrosis rats and suppressed both the phosphorylation of FAK and the phosphorylation of Akt simultaneously(P<0.01).At the same time,the expression of cyclinD1,collagen Ⅰ,and collagen Ⅲ was decreased by GFK significantly(P<0.01).Conclusions:CTGF and FAK/Akt signal pathway were activated in the CCl_4-induced hepatic fibrosis rats,which contribute to increased expression of cyclinD1 and collagen genes.The mechanisms of the anti-fibrosis activity of GFK may be due to its effects against CTGF and FAkIAkt signal pathway.
Objeclive: To investigate the effect of Ganfukang on connective tissue growth factor (CTGF) and focal adhesion kinase (FAK) / protein kinase B (PKB or Akt) signaling pathway in a hepatic fibrosis rat model and to explore the underlying therapeutic molecular mechanisms of GFK. Methods: Fifty SD rats were randomly divided into five groups as follows: the control group, the model group (repeated subcutaneous injection of CCl_4), and the three GFK treatment groups (31.25, 312.5, and 3125 mg / kg, intragastric administration). Reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting, and immunohistochemistry were used to examine the expression of CTGF, integrin α5, integrin β1, FAK / Akt signaling pathway, in the different-treated rats. Results: GFK attenuated the up-regulation of CTGF, integrin α5, and integrin β1 in hepatic fibrosis rats and suppressed both phosphorylation of FAK and the phosphorylation of Akt simultaneously (P <0.01). At the same time, the expression of (P <0.01) .Conclusions: CTGF and FAK / Akt signaling pathway were activated in the CCl_4-induced hepatic fibrosis rats, which contribute to increased expression of cyclin D1 and collagen genes. The mechanisms of the anti-fibrosis activity of GFK may be due to its effects against CTGF and FAkIAkt signal pathway.