二氢欧山芹通过调节自噬保护高糖诱导的足细胞损伤

    Columbianetin protects from high-glycemic podocyte damage by regulating autophagy

      摘要
    • 摘要: 目的 探讨二氢欧山芹（columbianetin，CBT）对高糖诱导的足细胞损伤保护作用及其机制研究。方法 体外培养永生化小鼠足细胞系MPC-5，给予高浓度的葡萄糖刺激，观察CBT对高糖诱导的足细胞损伤及自噬的影响；采用蛋白质印迹法检测足细胞自噬相关蛋白；荧光显微镜观察GFP-LC3-Ⅱ转染后足细胞绿色荧光颗粒。结果 高糖诱导足细胞损伤及自噬水平下降；CBT对高糖诱导的足细胞损伤具有显著保护作用，同时可上调自噬水平；CBT可上调TLR4、P-JNK的表达；siRNA TLR4及JNK抑制剂SP600125阻断CBT的保护作用。结论 CBT可调节足细胞自噬保护高糖造成的足细胞损伤，这一过程是通过促进TLR4/p-JNK信号通路实现的。

       

      Abstract: Objective To explore the protective effect of columbianetin(CBT)on the injury of podocytes induced by high glucose and its mechanism.Methods Immortalized murine foot cell line MPC-5 was cultured in vitro and the effects of CBT on injury and autophagy induced by high glucose were observed.Autophagy-related proteins were detected by Western blot.A fluorescent microscope was utilized for observing green fluorescent particles of GFP-LC3-Ⅱpodocyte after transfection.Results High glucose induced the injury of podocytes and decreased autophagy.CBT had a significant protective effect on the injury of podocytes induced by high glucose and could up-regulate autophagy.CBT up-regulated the expressions of TLR4 and p-JNK.siRNA TLR4 and inhibitor SP600125 blocked the protective effect of CBT.Conclusion CBT can induce autophagy in podocytes to protect podocytes from damage caused by high glucose.It is mediated by promoting TLR4/p-JNK signaling pathway.

       

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