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...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.展开更多
目的通过观察中药肝复康对肝纤维化大鼠肝组织金属蛋白酶组织抑制因子-1(tissue inhibitor of metalloproteinase-1,TIMP-1)表达的影响,探讨肝复康抗肝纤维化的可能机制。方法采用10%四氯化碳皮下注射制备肝纤维化模型,于造模第9周给予...目的通过观察中药肝复康对肝纤维化大鼠肝组织金属蛋白酶组织抑制因子-1(tissue inhibitor of metalloproteinase-1,TIMP-1)表达的影响,探讨肝复康抗肝纤维化的可能机制。方法采用10%四氯化碳皮下注射制备肝纤维化模型,于造模第9周给予肝复康治疗12周。通过测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST)活性及白蛋白和总蛋白的含量来反映肝脏功能,HE染色法观察肝组织病理学变化,免疫组化方法观察肝组织TIMP-1的表达。结果经肝复康治疗后,中剂量治疗组与模型组相比较,肝脏的组织学和血清学指标均明显改善,肝组织TIMP-1蛋白的表达显著减少(P<0.01)。结论肝复康对肝纤维化有疗效,其作用机制可能与降低肝组织TIMP-1蛋白的表达有关。展开更多
基金Supported by Natural Science Fund of Liaoning Province,China(No.201102055)
文摘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.
文摘目的通过观察中药肝复康对肝纤维化大鼠肝组织金属蛋白酶组织抑制因子-1(tissue inhibitor of metalloproteinase-1,TIMP-1)表达的影响,探讨肝复康抗肝纤维化的可能机制。方法采用10%四氯化碳皮下注射制备肝纤维化模型,于造模第9周给予肝复康治疗12周。通过测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST)活性及白蛋白和总蛋白的含量来反映肝脏功能,HE染色法观察肝组织病理学变化,免疫组化方法观察肝组织TIMP-1的表达。结果经肝复康治疗后,中剂量治疗组与模型组相比较,肝脏的组织学和血清学指标均明显改善,肝组织TIMP-1蛋白的表达显著减少(P<0.01)。结论肝复康对肝纤维化有疗效,其作用机制可能与降低肝组织TIMP-1蛋白的表达有关。
