›› 2017, Vol. 37 ›› Issue (7): 593-597.

• 基础研究 • 上一篇    下一篇

黄芪多糖对口腔扁平苔藓免疫调节机制的研究

马田田1,王秀梅2   

  1. 1. 哈尔滨医科大学附属第二医院
    2. 哈尔滨医科大学第二附属医院口腔牙体牙髓科
  • 收稿日期:2016-12-30 修回日期:2017-03-06 出版日期:2017-07-28 发布日期:2017-07-18
  • 通讯作者: 马田田 E-mail:821445827@qq.com
  • 基金资助:
    黑龙江省教育厅科学技术研究项目;黑龙江省人力资源和社会保障厅;哈尔滨市应用技术研究与开发项目

Study on the immunoregulation mechanism of Astragalus Polysaccharide in oral lichen planus

  • Received:2016-12-30 Revised:2017-03-06 Online:2017-07-28 Published:2017-07-18

摘要: 摘要] 目的  探讨黄芪多糖( Astragalus polysaccharide,APS)对口腔扁平苔藓(oral lichen planus,OLP)的免疫调节机制。方法 以LPS刺激HaCaT细胞建立体外OLP炎症模型,再以APS处理HaCaT细胞用逆转录聚合酶连技术检测核因子-κBP65(nuclear transcription factor kappa B,NF-kBp65)、Toll样受体4(Toll like receptor-4, TLR-4)、肿瘤坏死因子α(Tumor necrosis factor–α, TNF-α)、 白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6 )的mRNA表达情况;以MTT实验检测其对细胞的生长抑制率。结果 在体外OLP炎症模型中,NF-κBP65、TLR-4、TNF-α、IL-1β、IL-6 mRNA表达量明显下调,TLR-4及IL-1β的mRNA在6h时表达最低,NF-κBP65、TNF-α、IL-6的mRNA在24h时表达最低(P<0.001);25 μg/mlAPS作用24h对细胞的生长抑制最明显。结论 APS可能通过抑制TLR-4的激活,调控NF-κB的表达,也可能通过其他信号途径抑制炎症因子的表达,最终减轻OLP炎症反应与黏膜损伤。

关键词: 口腔扁平苔藓, 黄芪多糖, 免疫调节作用, TLRs/NF-κB

Abstract: Abstract: Objective To investigate the immunoregulation mechanism of Astragalus Polysaccharide in lichen planus. Methods  OLP inflammatory model was established by LPS stimulating HaCaT cells, and then the mRNA expressions of NF-κBP65,TLR-4,TNF-α,IL-1β,and IL-6 were detected by RT-PCR after APS treatment of HaCaT cells.The cell growth inhibition rate was detected by MTT assay. Results  In vitro OLP inflammation model, the mRNA expressions of NF-κBP65, TLR-4, TNF-α, IL-1β, IL-6 were significantly decreased. The mRNA expressions of TLR-4 and IL-1βin in 6h were the lowest, the mRNA expressions of NF-κBP65, TNF-α, IL-6 mRNA in 24h were the lowest (P<0.001). What inhibited cell growth most obviously was 25μg/mlAPS treated cells for 24h .Conclusions APS may inhibit the activation of TLR-4 to regulate the expression of NF-κB, and may also inhibit the expression of inflammatory factors through other signaling pathways, then ultimately alleviate the OLP inflammatory response and mucosal damage.

Key words: oral lichen planus, APS, immunoregulatory effect , TLRs/NF-κB

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