| 20-羟基蜕皮甾酮通过Akt/NF-κB通路调节小胶质细胞活化 |
| 投稿时间：2017-12-08 修订日期：2017-12-27 点此下载全文 |
| 引用本文：胡军,张彦海,潘娜,张佳,程妮,迟丽屹.20-羟基蜕皮甾酮通过Akt/NF-κB通路调节小胶质细胞活化[J].医学研究杂志,2018,47(10):79-83,99 |
| DOI：
10.11969/j.issn.1673-548X.2018.10.022 |
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| 基金项目:陕西省卫生计生科研基金资助项目（2016D061） |
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| 中文摘要:目的 观察20-羟基蜕皮甾酮对脂多糖诱导的体外原代培养小胶质细胞活化的影响，并探讨其相关机制。方法 脂多糖处理原代培养的SD大鼠小胶质细胞，构建其活化模型。实验分为正常组，脂多糖处理组和脂多糖+20-羟基蜕皮甾酮组。酶联免疫法测定各组细胞培养基中IL-1β和TNF-α的浓度，Western blot法检测各组细胞胞质内p-IκBα、细胞核内p-NF-κB以及细胞内p-Akt水平。结果 10ng/ml LPS孵育小胶质细胞8h，细胞培养基中IL-1β和TNF-α浓度分别从33.73±6.42pg/ml和43.67±7.17pg/ml上升至87.16±12.78pg/ml和96.55±13.76pg/ml （P<0.01）。50μmol/L 20-羟基蜕皮甾酮和LPS一起处理细胞8h后，笔者观察到细胞上清中IL-1β和TNF-α浓度分别降低至59.37±9.24和72.81±12.69pg/ml （P<0.05）。进一步增加20-羟基蜕皮甾酮浓度至100μmol/L，细胞上清中IL-1β和TNF-α浓度进一步降低至48.11±8.42pg/ml和61.44±9.38pg/ml （P<0.01）。此外，脂多糖导致小胶质细胞胞质内p-IκBα、细胞核内p-NF-κB和细胞内p-Akt水平明显升高（P<0.01），20-羟基蜕皮甾酮抑制上述蛋白水平的升高。结论 20-羟基蜕皮甾酮经Akt信号通路，失活NF-κB，抑制LPS诱导的小胶质细胞IL-1β和TNF-α分泌，最终改善小胶质细胞介导的炎症。 |
| 中文关键词:20-羟基蜕皮甾酮 小胶质细胞 炎症 NF-κB Akt |
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| 20-Hydroxyecdysone Inhibits Akt-Mediated NF-κB Activation in LPS-treated Microglial Cells |
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| Abstract:Objective To investigate the effects of 20-hydroxyecdysone on microglial activation and the related mechanisms in lipopolysaccharide(LPS)-stimulated microglial cells. Methods A model of activation of microglia was established by LPS in the primary cultured SD rat microglia. The experiment was divided into control group, LPS-treated group and LPS +20-hydroxyecdysone treated group. The concentration of IL-1β and TNF-α in the culture supernatant of microglia cells were determined by enzyme-linked immunosorbent assay in the experimental group. The levels of p-IκBα in the cytoplasm, p-NF-κB in the nucleus and p-Akt in cell were detected by Western blot. Results The concentration of IL-1β and TNF-α in the culture supernatant of microglia cells were increased from 33.73±6.42pg/ml and 43.67±7.17pg/ml up to 87.16±12.78pg/ml and 96.55±13.76pg/ml respectively after the microglia cells were treated by 10ng/ml LPS for 8 hours (P<0.01). We observed that the concentration of IL-1β and TNF-α in the culture supernatant of microglia cells were reduced to 59.37±9.24 and 72.81±12.69pg/ml after the microglia cells were treated by 50μmol/L 20-hydroxyecdysone and LPS for 8 hours (P<0.05). The concentration of IL-1β and TNF-α in the culture supernatant of microglia cells were further decreased to 48.11±8.42pg/ml and 61.44±9.38pg/ml respectively when The concentration of 20-hydroxyecdysone was increased to 100μmol/L (P<0.01). In addition, the levels of p-IκBα in the cytoplasm, p-NF-κB in the nucleus and p-Akt in cell were increased significantly in LPS-treated microglia cells, which were inhibited by 20-hydroxyecdysone. Conclusion 20-hydroxyecdysone caused inactivation of NF-κB via Akt signaling pathway, further inhibited the secretion of IL-1β and TNF-α of microglia and finally ameliorated the inflammatory responses of microglia induced by LPS. |
| keywords:20-Hydroxyecdysone Microglia Inflammation NF-κB Akt |
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