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

作者：张坤; 姜妙娜; 张彩华; 李骢; 贾玉杰

来源：Chinese Journal of Integrative Medicine, 2014, 20(06): 438-444.

• connective tissue growth factor
• Ganfukang
• hepatic fibrosis
• FAK/Akt signal pathway

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.

• 单位
  大连医科大学