番茄红素减轻高糖诱导小鼠足细胞损伤及其机制-东南大学学报医学版

番茄红素减轻高糖诱导小鼠足细胞损伤及其机制

单位：华中科技大学同济医学院附属武汉中心医院肾病内科, 湖北武汉 430000

分类号：R-33;R692

出版年·卷·期（页码）：2018·37·第二期（229-234）

摘要：

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.

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