中药肝复康对四氯化碳诱导的肝纤维化大鼠肝组织PI3K/PKB信号通路和PDGFR-β表达的影响

Effects of Gan-fu-kang on hepatic PI3K/ PKB signaling pathway and platelet-derived growth factor-β in rats with carbon tetrachloride-induced liver fibrosis

目的探讨中药肝复康对大鼠肝纤维化组织PI3K/PKB信号通路和血小板衍生生长因子受体-β(PDGFR-β)表达的影响。方法制备大鼠四氯化碳诱导的肝纤维化模型,给予肝复康干预。采用免疫组织化学法检测肝组织PDGFR-β蛋白的表达,采用半定量RT-PCR法测定肝组织PI3K和PKB1mRNA水平的变化。结果与对照组比,模型组肝组织PDGFR-β蛋白的表达上调,而肝复康治疗组其表达被显著抑制;模型组肝组织PI3K和PKB1 mRNA水平的相对光密度值分别为2.08±0.09和2.54±0.10,较对照组均显著上升(0.86±0.04和0.36±0.03,P<0.01),但肝复康治疗组其水平均被显著抑制(分别为0.88±0.05和0.41±0.03,与模型组比,P<0.01)。结论肝复康对肝纤维化的治疗作用可能与其作用于PI3K/PKB信号转导途径和抑制PDGFR-β表达有关。

Objective To investigate the effects of traditional Chinese herbal medicine Gan-fu-kang on hepatic PI3K/PKB signaling pathway and platelet-derived growth factor-β（PDGFR-β） in fibrotic liver in rats. Methods A rat model of liver fibrosis were induced by injection of 10%carbon tetrachloride （CCl4） subcuta-neously and was treated with Gan-fu-kang. The PDGFR-β protein in livers was detected by immunohistochem-istry and the PI3K and PKB1 mRNA were detected by semi-quantitive RT-PCR. Results The hepatic PDGFR-β protein in model animals was markedly increased than in the controls and was suppressed by Gan-fu-kang treatment;In the controls,the relative quantification value of PI3K and PKB1 mRNA were 0.86±0.04 and 0.36±0.03, respectively,which were significantly lower than that in the model animals （2.08±0.09 and 2.54±0.10,respectively,P〈0.01）; However,Gan-fu-kang treatment significantly inhibited the increased PI3K and PKB1 mRNA levels（0.88±0.05 and 0.41 ±0.03,respectively,P〈0.01） as compared to that in the models. Conclusion Gan-fu-kang may inhibit liver fibrosis by through inhibition of PI3K/PKB signaling pathway and PDGFR-β expression.