| 孟德姣,黄 玲,何慧敏,刘 璐,胡 雯.天麻素抑制脂多糖诱导的BV-2小胶质细胞炎症反应及机制研究[J].,2018,(6):1020-1023 |
| 天麻素抑制脂多糖诱导的BV-2小胶质细胞炎症反应及机制研究 |
| Inhibitory Effects of Gastrodin on LPS-induced Inflammatory Response on BV-2 Microglia Cells |
| 投稿时间：2017-10-18 修订日期：2017-11-14 |
| DOI：10.13241/j.cnki.pmb.2018.06.004 |
| 中文关键词: 天麻素 阿尔茨海默病 神经炎症 小胶质细胞 |
| 英文关键词: Gastrodin Alzheimer's disease Neuroinflammation Microglia |
| 基金项目:四川省医学科研青年创新课题（Q16016） |
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| 中文摘要: |
| 摘要 目的：研究天麻素对脂多糖（LPS）诱导的小胶质细胞炎性反应的影响，并探讨其潜在的作用机制。方法：BV-2小胶质细胞分为对照组、LPS组和天麻素组。LPS和天麻素处理24 h后，MTT和LDH试验检测细胞活性。ELISA实验检测炎性因子白介素-1β（IL-1β）、白介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）的含量。Western blot检测细胞中Iba-1和TLR4的表达，以及IκBα的降解和NFκB-P65的核转位情况。结果：LPS刺激后，BV-2细胞活性下降（65.46±3.70 %），LDH释放量增加（264.54±17.78 U/L），各炎性因子水平也显著升高。给予天麻素处理后，细胞活性升高（74.33±4.22 %），LDH释放量减少（173.88±15.23 U/L），炎性反应降低。同时，天麻素显著抑制LPS诱导的BV-2细胞Iba-1升高，降低了LPS处理后细胞TLR4的升高，IκBα的磷酸化水平和P65的核转位。结论：天麻素可以提高BV-2细胞活性，缓解LPS诱导的炎症反应。其作用机制可能是通过抑制BV-2细胞的过度活化，调控TLR4/NFκB信号通路，最终减少炎症因子的表达。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effect of gastrodin on inflammatory response of microglia induced by lipopolysaccharide (LPS) and to explore its potential mechanism. Methods: BV-2 microglia cells were divided into control group, LPS group and gastrodin group. 24 h after LPS and gastrodin treatment, MTT and LDH tests were performed to detect cell viability. ELISA assay was used to detect the levels of proinflammatory cytokines, including IL-1β, IL-6 and TNF-α. Western blot were carried out to detect the expression of Iba-1 and TLR4 in cells, and the degradation of IκBα and the nuclear translocation of NFκB-P65. Results: After the stimulation of LPS, the viability of BV-2 cells was decreased (65.46±3.70 %), and the levels of LDH were significantly increased (264.54±17.78 U/L), as well as the inflammatory cytokines. While after treatment with gastrodin, the cell viability was increased (74.33±4.22 %), the inflammatory reaction and LDH levels were decreased (173.88±15.23 U/L). At the same time, gastrodin significantly inhibited the expression of Iba-1 induced by LPS, and decreased the elevation of TLR4, the phosphorylation level of IκBα and the nuclear translocation of P65. Conclusion: Gastrodin can increase the viability of BV-2 cells and alleviate the inflammatory response induced by LPS. The underlying mechanism may be through inhibiting the over activation of BV-2 cells, regulating the TLR4/NFκB signaling pathway, and ultimately reducing the expression of proinflammatory cytokines. |
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