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 

机构地区：[1]Department of Pathophysiology,Dalian Medical University [2]Department of Pathophysiology Baotou Medical College

出　　处：《Chinese Journal of Integrative Medicine》2014年第6期438-444,共7页中国结合医学杂志（英文版）

基　　金：Supported by Natural Science Fund of Liaoning Province,China(No.201102055)

摘　　要：Objective： 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 α 5, integrin β 1, FAK/Akt signal pathway, cyclinD1, and collagen in the different-treated rats. Results： GFK attenuated the up-regulation of CTGF, integrin α 5, and integrin β 1 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 FAk/Akt signal pathway.Objective： 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 α 5, integrin β 1, FAK/Akt signal pathway, cyclinD1, and collagen in the different-treated rats. Results： GFK attenuated the up-regulation of CTGF, integrin α 5, and integrin β 1 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 FAk/Akt signal pathway.

关 键 词：connective tissue growth factor Ganfukang hepatic fibrosis FAK/Akt signal pathway 

分 类 号：R285.5[医药卫生—中药学]