Abstract | OBJECTIVE: 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.
|
Authors | Kun Zhang, Miao-na Jiang, Cai-hua Zhang, Cong Li, Yu-jie Jia |
Journal | Chinese journal of integrative medicine
(Chin J Integr Med)
Vol. 20
Issue 6
Pg. 438-44
(Jun 2014)
ISSN: 1993-0402 [Electronic] China |
PMID | 23990393
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
|
Chemical References |
- Drugs, Chinese Herbal
- Integrin alpha5
- Integrin beta1
- gan-fu-kang
- Cyclin D1
- Connective Tissue Growth Factor
- Collagen
- Focal Adhesion Protein-Tyrosine Kinases
- Proto-Oncogene Proteins c-akt
|
Topics |
- Animals
- Collagen
(genetics, metabolism)
- Connective Tissue Growth Factor
(genetics, metabolism)
- Cyclin D1
(genetics, metabolism)
- Drugs, Chinese Herbal
(pharmacology, therapeutic use)
- Female
- Focal Adhesion Protein-Tyrosine Kinases
(metabolism)
- Gene Expression Regulation
(drug effects)
- Integrin alpha5
(genetics, metabolism)
- Integrin beta1
(genetics, metabolism)
- Liver
(drug effects, enzymology, pathology)
- Liver Cirrhosis
(drug therapy, enzymology, genetics, pathology)
- Male
- Phosphorylation
(drug effects)
- Proto-Oncogene Proteins c-akt
(metabolism)
- Rats, Sprague-Dawley
- Signal Transduction
(drug effects)
|