中国结合医学杂志（英文版）Chinese Journal of Integrative Medicine

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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

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KeyWord:connective tissue growth factor, Ganfukang, hepatic fibrosis, FAK/Akt signal pathway

Author Name	Affiliation	E-mail
ZHANG Kun, JIANG Miao-na, ZHANG Cai-hua
JIA Yu-jie	Department of Pathophysiology, Dalian Medical University, Dalian, Liaoning Province (116044), China	pathophy2010@163.com

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Abstract:

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 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 FAk/Akt signal pathway.