上海交通大学学报（医学版）

上海交通大学学报（医学版）

• 论著（基础研究） • 上一篇    下一篇

丁基苯酞对脂多糖活化的小胶质细胞炎症介质释放的影响

支楠，徐群   

  1. 上海交通大学 医学院附属仁济医院神经内科，上海 200127
  • 出版日期:2016-12-28 发布日期:2016-12-29
  • 通讯作者: 徐群，电子信箱：xuqun628@163.com。
  • 作者简介:支楠（1986—），女，博士生；电子信箱：zhinanstudent@126.com。

Effects of d1-3-n-butylphthalide on the release of inflammatory mediators in lipopolysaccharide-activated microglia cells

ZHI Nan, XU Qun   

  1. Department of Neurology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China
  • Online:2016-12-28 Published:2016-12-29

PDF (PC)

991

摘要：

目的 ·观察丁基苯酞（NBP）对脂多糖（LPS）激活后的小胶质细胞炎症介质释放的影响。方法 ·原代培养大鼠脑皮质小胶质细胞和神经元，将接种后的小胶质细胞分为5组，即空白对照组、LPS激活组、溶剂+LPS组、0.01 mmol/L NBP+ LPS组以及0.1 mmol/L NBP+ LPS组。在LPS作用前2 h用NBP对小胶质细胞进行预处理，经LPS刺激24 h后在倒置显微镜下观察小胶质细胞形态；同时用酶联免疫吸附测定（ELISA）法检测各组小胶质细胞释放的炎症因子肿瘤坏死因子-α（TNF-α）、白介素-1β（IL-1β）及白介素-10（IL-10）含量；用硝酸还原法检测一氧化碳（NO）含量；经四甲基偶氮唑盐(MTT)法检测经各组作用后的神经元存活率。结果 · NBP预处理后的小胶质细胞经LPS刺激后仍呈激活形态，NBP不影响激活的小胶质细胞释放炎症因子TNF-α、IL-1β以及 IL-10，但可抑制其释放炎症介质NO，提高神经元存活率，并呈现剂量依赖性。结论 · NBP可减轻小胶质细胞经LPS活化后的神经炎症反应，并具有剂量依赖性的神经保护作用。

关键词: 丁基苯酞, 小胶质细胞, 炎症

Abstract:

Objective · To investigate the effects of d1-3-n-butylphthalide (NBP) on inflammatory mediators released by microglia cells after being activated with lipopolysaccharide (LPS). Methods · Microglia cells and neurons were obtained from primary cultured rat cortices. Microglia cells were divided into five groups, including the blank control group, the LPS activated group, the solvent plus LPS group, the 0.01 mmol/L NBP plus LPS group, and the 0.1 mmol/L NBP plus LPS group. Microglia cells were pretreated with NBP 2 h before LPS stimulation. The morphology of microglia cells was observed under inverted microscope after being stimulated with LPS for 24 h. The levels of inflammatory factors, including tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and interleukin 10 (IL-10), were measured with enzyme linked immunosorbent assay (ELISA) method and the content of carbon monoxide (NO) was measured using nitrate reductase method. The survival rate of neurons was detected by MTT method. Results · NBP pretreated microglia cells remained the activated form after LPS stimulation. NBP did not affect the release of TNF-α, IL-1β, and IL-10 by activated microglia cells, but inhibited the production of inflammatory mediator NO, thus improved the survival rate of neurons in a dose-dependent manner. Conclusion · NBP can attenuate the LPS-induced neuroinflammatory responses in microglia cells and show the dose-dependent neuroprotection.

Key words: d1-3-n-butylphthalide, microglia, inflammation