TITLE

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

AUTHOR(S)
Zhang, Kun; Jiang, Miao-na; Zhang, Cai-hua; Li, Cong; Jia, Yu-jie
PUB. DATE
June 2014
SOURCE
Chinese Journal of Integrative Medicine;Jun2014, Vol. 20 Issue 6, p438
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
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 CCl), 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-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.
ACCESSION #
96701361

 

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