番茄红素减轻高糖诱导小鼠足细胞损伤及其机制

Lycopene relieves the damage of mouse podocytes induced by high glucose and its mechanism

目的:探究番茄红素(Lyc)对高糖诱导小鼠肾足细胞(MPC5)损伤的保护作用及机制。方法:体外培养MPC5细胞,使用高糖和不同剂量(3.125、6.25、12.5μmol·L-1)Lyc处理细胞,采用MTT和流式细胞术分别检测细胞活性和胞内活性氧(ROS)含量,Western blot检测细胞损伤标志蛋白、自噬相关蛋白和磷脂酰肌醇3激酶/蛋白激酶B(PI3K/AKT)通路蛋白的表达。结果:与正常糖组比较高糖组MPC5细胞活性降低,胞内ROS含量增加(P<0.05)。Lyc可增加高糖状态下MPC5的细胞活性,且具有剂量依赖性;Lyc还可清除胞内ROS,诱导自噬增加,改善细胞损伤,活化PI3K/AKT通路,均与高糖组有显著差异(P<0.05)。与高糖+高剂量Lyc组比较,LY294002处理后细胞中PI3K/AKT通路蛋白表达被抑制,细胞自噬降低,细胞损伤增加(P<0.05)。结论:Lyc可通过降低胞内ROS增强自噬,减轻高糖诱导小鼠MPC5损伤,这一作用机制可能与PI3K/AKT信号通路有关。

Objective:To investigate the protective effect and mechanism of lycopene(Lyc)on damage of mouse podocytes(MPC5)induced by high glucose.Methods:MPC5 were cultured in vitro and treated with high glucose and different doses of Lyc(3.125,6.25,12.5μmol·L-1).Then cell viabilties and intracellular ROS content were detected by MTT and flow cytometry,respectively;and the expression levels of marker proteins for cell damage,autophagy related proteins and some key proteins involved in phosphatidylinositol 3 kinase/protein kinase B(PI3K/AKT)signaling pathway were detected by Western blot.Results:Compared with that in normal glucose group,cell viability of MPC5 cells in high glucose group decreased while the ROS content increased in high glucose group(P<0.05).Lyc increased cell viability of MPC5 cells in high glucose state,and this effect was dose-dependent.Lyc treatment could decrease intracellular ROS contents,induce autophagy increasing,improve cell damage and activate PI3K/AKT signaling pathway.Compared with those in high glucose group,all of those differences were significant(P<0.05).Compared with high glucose and high dose of Lyc group,the expression levels of proteins involved in PI3K/AKT pathway were inhibited,cell autophagy decreased,cell injury increased(P<0.05)after the treatment with LY294002.Conclusion:Lyc can relieve the damage of MPC5 induced by high glucose through reducing the ROS content and enhancing the autophagy of MPC5 cells,which the mechanism may be related to PI3K/AKT signaling pathway.