Effects of Ganfukang(肝复康) on Expression of Connective Tissue Growth Factor and Focal Adhesion Kinase/Protein Kinase B Signal Pathway in Hepatic Fibrosis Rats

【摘要】 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 CCl₄）,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 CCl₄-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.更多还原

【Abstract】 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 CCl₄）,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 CCl₄-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.更多还原