口腔医学研究 ›› 2020, Vol. 36 ›› Issue (12): 1123-1127.DOI: 10.13701/j.cnki.kqyxyj.2020.12.010

• 牙周病学研究 • 上一篇    下一篇

高糖对牙龈卟啉单胞菌LPS引发牙周膜细胞炎症反应的影响

孙天祥1,2, 苗棣1,2*, 王宝彦2, 陈悦2   

  1. 1.西安交通大学口腔医院陕西省颅颌面精准医学研究重点实验室 陕西 西安 710004;
    2.西安交通大学口腔医院牙周黏膜科 陕西 西安 710004
  • 收稿日期:2020-04-13 出版日期:2020-12-28 发布日期:2020-12-28
  • 通讯作者: *苗棣, E-mail: corchorus@hotmail.com
  • 作者简介:孙天祥(1991~ ),男,山东菏泽人,硕士,住院医师,主要从事牙周病的临床和基础研究。
  • 基金资助:
    国家自然科学基金青年科学基金项目(编号:81700986)

Impact of High Glucose on Porphyromonas Gingivalis LPS induced Inflammation of Periodontal Ligament Cells

SUN Tianxiang1,2, MIAO Di1,2*, WANG Baoyan2, CHEN Yue2   

  1. 1. Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, Hospital of Stomatology, Xi'an Jiaotong University, Xi'an 610041, China;
    2. Department of Periodontics and Oral Mucosa Diseases, Hospital of Stomatology, Xi'an Jiaotong University, Xi'an 610041, China
  • Received:2020-04-13 Online:2020-12-28 Published:2020-12-28

摘要: 目的:观察高糖对牙龈卟啉单胞菌(Porphyromonas gingivalis,P.gingivalis)重要毒力因子脂多糖(lipopolysaccharide,LPS)引发宿主牙周膜细胞释放炎症细胞因子和对核因子-κB (Nuclear factor-κB,NF-κB)表达、活化的影响。方法:人牙周膜细胞(human periodontal ligament cells,hPDLCs)培养于葡萄糖生理浓度中作为对照组,P.gingivalis LPS (1 μg/mL)、高糖(25 mmol/L)、高糖+P.gingivalis LPS刺激细胞6 h和12 h后,酶联免疫吸附法(enzyme linked immunosorbent assay,ELISA)检测上清液中白细胞介素-1β(Interleukin-1β,IL-1β)和肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的释放,实时荧光定量PCR(quantitative real time PCR, qRT-PCR)和Western-blot检测NF-κB p65和磷酸化NF-κB p65(phospho-NF-κB p65, p-NF-κB p65)在hPDLCs中的表达水平。结果:高糖和P.gingivalis LPS可分别促进hPDLCs表达IL-lβ和TNF-α、促进NF-κB p65表达和活化,高糖和P.gingivalis LPS的共刺激可以增强这一促进作用。结论:高糖可能通过对NF-κB的活化增强P.gingivalis LPS致hPDLCs的炎症作用。

关键词: 牙龈卟啉单胞菌, 脂多糖, 高糖, 牙周炎, 糖尿病

Abstract: Objective: To investigate the impact of high glucose on inflammatory mediators release and NF-κB expression and on activation of human periodontal ligament cells induced by P.gingivalis lipopolysaccharide. Methods: Primary cultured hPDLCs were challenged in P.gingivalis LPS (1μg/mL), high glucose (25mmol/L), and high glucose+P.gingivalis LPS for 6 and 12 hours. The hPDLCs were cultured in physical concentration of glucose as control. The expression of TNF-α and IL-1β were detected by ELISA. The expression of NF-κB p65 and p-NF-κB p65 were measured by qRT-PCR and western-blot. Results: High glucose and P.gingivalis LPS could promote the expression of inflammatory cytokines TNF-α and IL-1β, and promote the expression and activation of NF-κB p65 in hPDLCs. The co-stimulation of high glucose and P.gingivalis LPS could enhance the expression of inflammatory cytokines and activation of NF-κB p65. Conclusion: High glucose may enhance the inflammation induced by P. gingivalis LPS through activation of NF-κB.

Key words: Porphyromonas gingivalis, lipopolysaccharide, high glucose, periodontitis, diabetes