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中国临床药理学与治疗学 ›› 2018, Vol. 23 ›› Issue (2): 126-131.doi: 10.12092/j.issn.1009-2501.2018.02.002

• 基础研究 • 上一篇    下一篇

酸枣仁皂苷A对脂多糖诱导小胶质细胞活化的影响及神经保护作用

张 睿,李冰洁,李庆林   

  1. 安徽中医药大学科研实验中心,安徽中医药大学新安医学教育部重点实验室,合肥 230038,安徽
  • 收稿日期:2017-09-01 修回日期:2017-10-10 出版日期:2018-02-26 发布日期:2018-03-02
  • 通讯作者: 李庆林,男,博士,教授,研究方向:分子药理学。 Tel: 0551-65169371 E-mail: qinglin_lee@hotmail.com
  • 作者简介:张睿,女,硕士,研究方向:分子药理学。 Tel: 0551-65169371 E-mail: zrui2568@163.com
  • 基金资助:

    国家自然科学基金(30973894)

Jujuboside A attenuates LPS-induced microglial activation and provides neuroprotection

ZHANG Rui, LI Bingjie, LI Qinglin   

  1. Experimental Research Center, Anhui University of Chinese Medicine; Key Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei 230038, Anhui, China
  • Received:2017-09-01 Revised:2017-10-10 Online:2018-02-26 Published:2018-03-02

摘要:

目的: 研究酸枣仁皂苷A(Ju A)对脂多糖(LPS)诱导BV-2小胶质细胞神经炎症发生的影响及神经炎症导致的神经元细胞损伤的保护作用。 方法: 以LPS(1 μg/mL)刺激BV-2小胶质细胞24 h建立神经炎症模型,采用不同浓度的Ju A(2.5、5、10 μmol/L)进行干预。MTT法检测Ju A单独及联合LPS对BV-2细胞存活率的影响;Griess法检测Ju A对激活的BV-2细胞NO释放的影响;ELISA法检测BV-2细胞上清液中TNF-alfa、IL-1beta分泌水平;DCFH-DA探针法检测BV-2细胞内ROS水平;MTT法检测Ju A干预后的BV-2条件培养基对正常小鼠海马神经元细胞(HT-22)存活率的影响。结果: MTT结果显示,Ju A在浓度范围内对BV-2的存活率无明显影响。Griess和ELISA实验结果表明,Ju A可抑制激活的BV-2细胞NO、TNF-alfa、IL-1beta释放水平,同时Ju A还可抑制细胞内ROS水平。此外,Ju A干预的BV-2条件培养基可抑制神经炎症对HT-22海马神经元细胞的损伤。结论: Ju A可在体外抑制LPS诱导的BV-2细胞的炎症发生并保护HT-22细胞因神经炎症受到的损伤。

关键词: 酸枣仁皂苷A, 小胶质细胞, 海马神经元细胞, 神经炎症, 神经保护

Abstract:

AIM: To investigate the inhibitory effects of Jujuboside A (Ju A) on LPS induced inflammation mediators in BV-2 microglial cells, and the neuroprotective effect of Ju A in neuronal injury.  METHODS: BV-2 cells were pre-treated with Ju A, and then stimulated by LPS. The cell viabilities were measured by MTT assay, the levels of NO were measured by Griess assay, the concentrations of TNF-alfa, IL-1beta were detected by using ELISA, the contents of ROS were detected by DCFH-DA probe method, and the effect of BV-2 conditioned medium on survival rate of HT-22 cells was detected by MTT. RESULTS:Ju A had no significant effect on cell viability within  tested concentrations.Ju A significantly inhibited the production of NO, TNF-alfa, IL-1beta and ROS. BV-2 conditioned medium intervened by Ju A inhibited the neuroinflammation on HT-22 hippocampal neuron cells. CONCLUSION: Ju A inhibits LPS-induced microglia activation and neuroinflammation, which mediates its neuroprotective effect on neuronal injury.

Key words: Jujuboside A, microglial cell, hippocampal neurons, neuroinflammation, neuroprotective

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