摘要
探讨人胰岛素样生长因子-1(IGF-1)的体外抗肝纤维化作用。检测IGF-1对人正常肝细胞L-02增殖及生长周期的影响;建立CCl_4诱导的肝细胞损伤模型,探究IGF-1抗肝细胞损伤活性;以TGF-β1诱导的肝星状细胞HSC-T6为体外肝纤维化研究模型,检测IGF-1对HSC-T6细胞中纤维化相关蛋白表达水平及对胞内TGF-β1/Smad信号通路的影响。结果显示,IGF-1可解除TGF-β1对L-02生长的抑制作用,提高CCl4损伤L-02的细胞存活率,降低HSC-T6细胞纤维化相关蛋白表达水平,抑制TGF-β1/Smad信号通路中Smad3的磷酸化。结果表明,IGF-1能够促进肝细胞增殖,保护肝细胞免受损伤,干预TGF-β1/Smad信号通路,抑制胞外基质ECM合成,从而发挥抗肝纤维化效果。
This study was focus on investigating the anti-liver fibrosis effects of insulin-like growth factor-1 （IGF- 1） in vitro. The effects of IGF-1 on human liver L-02 cell viability and cell cycle were observed. CC14-induced L- 02 cell injury was set up to detect the anti-apoptotic activity of insulin-like growth factor-1 （IGF-1）. Transforming growth factor ｜B1 （TGF-｜B1） induced hepatic stellate cell line （ HSC-T6） were used as a liver fibrosis model in vitro to analyze the effects of IGF-1 on the expression of liver fibrosis proteins and intracellular TGF-｜Bl/Smad signaling pathway in HSC-T6 cells. The results showed that IGF-1 could relieve the growth inhibition effects of TGF-｜B1 on L-02 cells, increase the viability of L-02 cells injured by CC14, decrease the expression of liver fibrosis proteins, and inhibit the TGF-｜Bl/Smad signaling pathway by inhibiting the phosphorylation of Smad3. Our study suggested that IGF-1 exerted anti-liver fibrosis effects by stimulating L-02 cells proliferation, reducing cell damage and inhibiting ECM accumulation via interfering TGF-｜Bl/Smad signaling pathway.
出处
《中国药科大学学报》
CAS
CSCD
北大核心
2017年第4期476-482,共7页
Journal of China Pharmaceutical University
基金
国家高技术研究发展计划(863计划)资助项目(No.2014AA021003)
江苏省优势学科建设工程资助项目(PADA)~~
