›› 2017, Vol. 37 ›› Issue (1): 25-28.

• 基础研究 • 上一篇    下一篇

茶多酚抑制过氧化氢诱导的牙周膜细胞损伤

刘彩宏,呼海燕   

  1. 延安大学附属医院
  • 收稿日期:2016-01-21 修回日期:2016-04-08 出版日期:2017-01-28 发布日期:2017-01-17
  • 通讯作者: 刘彩宏 E-mail:caihongliuya@163.com

Inhibitory effect of tea polyphenols on H2O2 induced human periodontal ligament cell injury

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  • Received:2016-01-21 Revised:2016-04-08 Online:2017-01-28 Published:2017-01-17

摘要: 目的 探讨茶多酚(Tea polyphenols,TP)对过氧化氢(H2O2)诱导的牙周膜细胞损伤的保护作用及其机制。方法 构建H2O2诱导牙周细胞损伤模型。细胞随机分为正常对照组、H2O2组、H2O2+TP组。MTT检测细胞活力,流式细胞仪检测细胞凋亡。试剂盒检测各组细胞中丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性。Western blot检测细胞中caspase3、caspase12、Bcl2和Bax的表达。Elisa检测细胞中IL1β和IL6的表达情况。结果 H2O2处理会降低牙周膜细胞的活性,并且浓度越高,细胞活性降低越明显。茶多酚可抑制在H2O2介导下牙周膜细胞的活性降低、凋亡升高,MDA含量增加,SOD活性降低,caspase3、caspase12和Bax的表达升高,Bcl2的表达降低,以及IL1β和IL6的表达增高。结论 茶多酚对H2O2诱导的牙周膜细胞损伤有明显的保护作用,其机制与减轻细胞氧化应激损伤、抑制线粒体凋亡通路和降低细胞炎性水平有关。

关键词: 红景天苷, 牙周膜细胞

Abstract: Abstract: Objective To study the protective effect of tea polyphenols (TP) on H2O2 induced human periodontal ligament cell injury and its mechanism. Methods Human periodontal ligament cell injury model was established using H2O2. Cells were randomly divided into three groups: control group, H2O2 group, and H2O2+ TP group. Cell viability was detected using MTT method and cell apoptosis was detected by flow cytometry. The MDA content and SOD activity were measured by the MDA and SOD detection kit. Protein expression levels of caspase-3, caspase-12, Bcl-2 and Bax were examined by western blot. The expression of IL-1β and IL-6 was detected by ELISA method. Results The cell viability was decreased with H2O2 treatment in a dose dependent manner. TP reversed the effect of H2O2 in human periodontal ligament cells, which included decrease of cell viability, increase of cell apoptosis, elevation of MDA, reduction of SOD activity, increase of expression levels of caspase-3, caspase-12, and Bax, decrease of Bcl-2 expression, and elevation of IL-1β and IL-6 expression. Conclusion The TP treatment protects H2O2 induced human periodontal ligament cell injury via inhibiting oxidative stress, mitochondrial apoptotic pathways and inflammation.

Key words: salidroside, periodontal ligament cells

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