姜黄素通过抑制IGF2/NF-κB改善ox-LDL诱导的细胞损伤

    Curcumin improves ox-LDL-induced cell damage by inhibiting IGF2/NF-κB

      摘要
    • 摘要:
      目的  探究姜黄素通过抑制胰岛素样生长因子2（insulin-like growth factor 2，IGF2）缓解氧化低密度脂蛋白（oxidized low-density lipoprotein，ox-LDL）诱导的细胞损伤的分子机制，以阐明姜黄素治疗动脉粥样硬化的分子机制。
      方法  通过ox-LDL处理人脐静脉内皮细胞（human umbilical vein endothelial cells，HUVECs）构建细胞模型，通过实时荧光定量聚合酶链反应（quantitative real-time polymerase chain reaction，qRT-PCR）检测IGF2 mRNA的表达水平；CCK8和EdU检测细胞活力和增殖水平；流式细胞术检测细胞凋亡比率；蛋白免疫印迹检测IGF2、Bax和Bcl-2蛋白水平；酶联免疫吸附法测定TNF-α、IL-1β和IL-6的浓度。
      结果  与对照组相比，ox-LDL组IGF2 mRNA和蛋白表达升高（P<0.05，P<0.01），细胞增殖水平降低（P<0.01），细胞凋亡率升高（P<0.01），Bax水平升高，Bcl-2水平降低（P<0.01）；TNF-α、IL-1β和IL-6浓度升高（P<0.01）；p-p65/p65蛋白水平升高（P<0.01）。ox-LDL+姜黄素组较ox-LDL组IGF2 mRNA和蛋白表达降低（P<0.05，P<0.01），细胞增殖水平升高（P<0.01），细胞凋亡率降低（P<0.05），Bax水平降低（P<0.01），Bcl-2水平升高（P<0.05）；TNF-α、IL-1β和IL-6浓度降低（P<0.05，P<0.01）；p-p65/p65蛋白水平降低（P<0.01）。ox-LDL+姜黄素+oe-IGF2组较ox-LDL+姜黄素组IGF2 mRNA和蛋白表达升高（P<0.01），细胞增殖水平降低（P<0.01），细胞凋亡率增加（P<0.05），Bax水平升高，Bcl-2水平降低（P<0.01）；TNF-α、IL-1β和IL-6浓度升高（P<0.05，P<0.01）；p-p65/p65蛋白水平升高（P<0.01）。
      结论  姜黄素通过抑制IGF2介导的NF-κB通路缓解ox-LDL诱导的细胞凋亡和炎症反应。

       

      Abstract:
      AIM  To explore the molecular mechanism of curcumin in alleviating oxidative low-density lipoprotein (ox-LDL) induced cell damage by inhibiting insulin-like growth factor 2 (IGF2), so as to elucidate the role of curcumin in treating atherosclerosis.
      METHODS  Cell model was created by ox-LDL induced Human umbilical vein endothelial cells (HUVECs), and the expression level of IGF2 mRNA was detected by qRT-PCR. CCK8 and EdU were used to detect cell viability and proliferation. The apoptosis rate was measured by flow cytometry. The levels of IGF2, Bax and Bcl-2 were tested by Western blotting. The concentrations of TNF-α, IL-1β and IL-6 were determined by ELISA.
      RESULTS  Compared with the control group, IGF2 mRNA and protein level in ox-LDL group were increased (P<0.05, P<0.01), together with decreased cell proliferation level (P<0.01). The results also reported increased apoptosis rate (P<0.01), increased Bax protein level, as well as decreased Bcl-2 protein level (P<0.01); The observation also included increased concentrations of TNF-α, IL-1β and IL-6 (P<0.01), coupled with increased p-p65/p65 level (P<0.01). Compared with ox-LDL group, the group of ox-LDL with added curcumin showed decreased IGF2 mRNA and protein level (P<0.05, P<0.01), increased cell proliferation level (P<0.01), decreased cell apoptosis rate (P<0.05), decreased Bax protein level (P<0.01) and elevated Bcl-2 protein level (P<0.05); The concentrations of TNF-α, IL-1β and IL-6 dropped (P<0.05, P<0.01); The p-p65/p65 level was decreased (P<0.01). In comparison, the ox-LDL+ curcumin +oe-IGF2 group showed increased IGF2 mRNA and protein expression (P<0.01), reduced cell proliferation level (P<0.01), and the rise of cell apoptosis rate (P<0.05) and Bax protein level (P<0.01). Bcl-2 protein level declined (P<0.01); The concentrations of TNF-α, IL-1β and IL-6 were increased (P<0.05, P<0.01); The p-p65/p65 level was elevated (P<0.01).
      CONCLUSION  Curcumin alleviates ox-LDL-induced apoptosis and inflammation by inhibiting IGF2-mediated NF-κB pathway.

       

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