上海口腔医学

上海口腔医学 ›› 2020, Vol. 29 ›› Issue (5): 462-465.doi: 10.19439/j.sjos.2020.05.003

• 论著 • 上一篇    下一篇

牡荆素对脂多糖诱导牙髓干细胞表达炎症因子的影响

牛晨光, 李佳洋, 於丽明, 陈栋, 韦晓玲   

  1. 上海市口腔病防治院,复旦大学附属口腔医院 口腔生物医学工程实验室,上海 200001
  • 收稿日期:2019-11-29 修回日期:2020-04-20 出版日期:2020-10-25 发布日期:2020-11-02
  • 通讯作者: 韦晓玲,E-mail：xiaoling_wei@fudan.edu.cn
  • 作者简介:牛晨光（1989-）,男,硕士,住院医师,E-mail：niuchg09@alumni.sjtu.edu.cn
  • 基金资助:
    上海市卫生和计划生育委员会科研课题(201740051)

Influence of vitexin on the expression of inflammatory cytokines in dental pulp stem cells induced by lipopolysaccharide

NIU Chen-guang, LI Jia-yang, YU Li-ming, CHEN Dong, WEI Xiao-ling   

  1. Oral Biomedical Engineering Laboratory, Shanghai Stomatological Hospital, Fudan University. Shanghai 200001, China
  • Received:2019-11-29 Revised:2020-04-20 Online:2020-10-25 Published:2020-11-02

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摘要： 目的：探讨牡荆素（vitexin,VTX）对脂多糖（lipopolysaccharide,LPS）诱导的人牙髓干细胞（human dental stem pulp cells,hDPSCs）表达炎症因子的影响,并初步探讨其相关作用机制。方法：分离、培养hDPSCs,以CCK-8法检测VTX对hDPSCs增殖的影响,检测VTX毒性浓度范围。铺种hDPSCs,分为4组,空白组以不含LPS和VTX的无血清DMEM,LPS组仅加入含LPS终浓度为2 μg/mL的无血清DMEM培养,VTX处理组1(V1组)加入2 μg/mL LPS+25 μmol/L VTX,VTX处理组2(V2组)加入2 μg/mL LPS + 50 μmol/L VTX。培养48 h,实时荧光定量PCR检测各组细胞中IL-1β、IL-6及IL-8基因转录,蛋白质免疫印迹检测hDPSCs内MPAK信号通路及COX-2等蛋白的变化。采用SPSS 16.0软件包对数据进行统计学分析。结果：VTX在200 μmol/L范围内时细胞活力不受影响(P>0.05);VTX抑制LPS刺激hDPSCs转录IL-1β、IL-6及IL-8,抑制效果与VTX的浓度呈正相关;VTX可显著抑制LPS激活p38及ERK信号通路。结论：VTX可能通过抑制p38及ERK信号通路的激活,降低LPS诱导的hDPSCs转录IL-1β、IL-6及IL-8。

关键词: 牡荆素, 人牙髓干细胞, 炎症因子, MAPK

Abstract: PURPOSE: To investigate the effect of vitexin (VTX) on the expression of inflammatory cytokines in human dental pulp stem cells(hDPSCs) induced by lipopolysaccharide(LPS), and to explore the underlying mechanism. METHODS: hDPSCs were isolated and cultured, and CCK-8 method was used to detect the effect of VTX on proliferation of hDPSCs. hDPSCs were randomly divided into 4 groups: blank group (without LPS and VTX),LPS group (2 μg/mL LPS),2 μg/mL LPS + 25 μmol/L VTX,2 μg/mL LPS + 50 μmol/L VTX. The cells of all groups were cultured for 48 h. The gene levels of IL-1β, IL-6 and IL-8 in hDPSCs were detected by real time qPCR(RT-qPCR). The change of COX-2 and MAPKs signaling pathways were detected by Western blot. SPSS 16.0 software package was used for statistical analysis. RESULTS: When the VTX concentration was less than 200 μmol/L, the cell viability was not affected(P>0.05). VTX at 25 and 50 μmol/L significantly reduced LPS-induced expression of IL-1β, IL-6 and IL-8 at gene levels and COX-2 at protein level (P<0.05). CONCLUSIONS: VTX significantly inhibited the activation of ERK and p38 signaling pathway. VTX can reduce LPS-induced inflammatory cytokine expression in hDPSCs via restraining the activation of ERK and p38 signaling pathway.

Key words: Vitexin, Human dental pulp stem cells, Inflammatory cytokine, MAPKs

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