葫芦素B调控IGFBPrP1抗小鼠肝纤维化的作用及机制研究

Effect and mechanism of cucurbitacin B on anti-liver fibrosis in mice via regulating IGFBPrP1

目的:探讨葫芦素B调控胰岛素样生长因子结合蛋白相关蛋白1(IGFBPrP1)抗小鼠肝纤维化的作用及机制。方法:将ICR小鼠经尾静脉注射12.5 mg/kg的Con A溶液构建肝纤维化模型,将其分为葫芦素B组和模型组,另选正常ICR小鼠为正常组。葫芦素B组小鼠同时给予葫芦素B灌胃,正常组和模型组给予等量生理盐水灌胃。小鼠末次给药后采集静脉血,经酶联免疫吸附测定法(ELISA)检测透明质酸(HA)、层粘蛋白(LN)、Ⅲ型前胶原(PCⅢ)及Ⅳ型胶原(Ⅳ-C)水平;并比较肝组织中转化生长因子-β1(TGF-β1)和IGFBPrP1水平。结果:模型组和葫芦素B组血清HA,LN,PCⅢ及Ⅳ-C明显高于正常组,葫芦素B组低于模型组,差异有统计学意义(P<0.05)。模型组和葫芦素B组小鼠肝组织中TGF-β1和IGFBPrP1水平均明显高于正常组(P<0.05),而葫芦素B组明显低于模型组,差异均有统计学意义(P<0.05)。结论:葫芦素B能调控IGFBPrP1和TGF-β1水平抗小鼠肝纤维化。

Objective:To investigate the effect of cucurbitacin B on liver fibrosis in mice by regulating insulin-like growth factor binding protein-related protein 1(IGFBPrP1).Methods:Liver fibrosis model was established by intravenous injection of 1 g/L of Con A solution through tail vein for ICR mice,divided into model group and cucurbitacin B group,another normal ICR mouse was selected as the normal group.Cucurbitacin B group mice were given cucurbitacin B by gavage at the same time.Normal group and model group were given the same amount of saline by gavage.The levels of haluronic acid(HA),laminin(LN),procollagen type Ⅲ(PCⅢ)and collagen Ⅳ(Ⅳ-C)were detected by enzyme-linked immunosorbent assay(ELISA),and the levels of transforming growth factor-β1(TGF-β1)and IGFBPrP1 in liver tissue were compared.Results:Serum HA,LN,PCⅢandⅣ-C in model group and cucurbitacin B group were significantly higher than normal group,cucurbitacin B group lower than model group,there was significient difference(P<0.05).The levels of IGFBPrP1 and TGF-β1 in liver tissue of mice in cucurbitacin B group and model group higher than normal group,cucurbitacin B group lower than model group,there was significient difference(P<0.05).Conclusion:Cucurbitacin B can anti-liver fibrosis by regulating the levels of IGFBPrP1 and TGF-β1 in mice.