口腔医学研究

口腔医学研究 ›› 2017, Vol. 33 ›› Issue (7): 698-702.DOI: 10.13701/j.cnki.kqyxyj.2017.07.003

• 基础研究论著 • 上一篇    下一篇

PPARγ在脂多糖刺激牙周膜细胞中调控NF-κB信号通路的作用研究

杨芳1,3, 陈明月2, 胡英英1,3, 汪昌宁1,3*   

  1. 1. 武汉大学口腔医学院·湖北省口腔基础医学重点实验室-省部共建国家重点实验室培育基地·武汉大学口腔生物医学教育部重点实验室 湖北 武汉 430079;
    2. 十堰市太和医院口腔科 湖北 十堰 442000;
    3. 武汉大学口腔医院牙周科 湖北 武汉 430079
  • 收稿日期:2017-01-16 出版日期:2017-07-20 发布日期:2017-07-27
  • 通讯作者: 汪昌宁,E-mail: wangcn@whu.edu.cn
  • 作者简介:杨芳(1989~ ),女,湖北省咸宁市人,硕士在读,主要从事牙周病学相关的研究工作。
  • 基金资助:
    国家自然科学基金资助项目(编号: 30973314)

PPARγ Regulating NF-κB Signaling Pathway in Lipopolysaccharide-induced Human Periodontal Ligament Cells.

YANG Fang1, CHEN Ming-yue2, HU Ying-ying1, WANG Chang-ning1,3*.   

  1. 1. The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, School of Stomatology, Wuhan University, Wuhan 430079, China;
    2. Department of Stomatology, Hospital of Taihe, Shiyan 442000, China;
    3. Department of Periodontology, Hospital of Somatology, Wuhan University, Wuhan 430079, China.
  • Received:2017-01-16 Online:2017-07-20 Published:2017-07-27

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摘要： 目的:探讨PPARγ在牙周炎中调控作用机制。方法:组织块法培养健康人牙周膜细胞(human periodontal ligament cells, hPDLCs)并鉴定。细胞处理分为以下4组,A组:对照组;B组:脂多糖(lipopolysaccharide,LPS )刺激组;C组:罗格列酮对照组,即二甲基亚砜(dimethylsulfoxide, DMSO)处理组;D组:罗格列酮处理组。免疫印迹法检测过氧化物酶体增殖物激活受体γ(peroxisome proliferator activated receptor γ,PPARγ)和核因子κB(nuclear factor κB, NF-κB) p65胞核、胞浆及总蛋白含量,细胞免疫荧光检测NF-κB p65表达部位。实时定量PCR和酶联免疫法检测白细胞介素1β(interleukin-1β,IL-1β)和肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)RNA和蛋白表达。结果:LPS刺激下,胞核PPARγ表达降低NF-κB p65表达升高,相应的IL-1β和TNF-α RNA及蛋白表达量均升高。同时加入罗格列酮后,胞核PPARγ表达升高NF-κB p65表达降低,且IL-1β和TNF-α RNA及蛋白表达量均降低。差异均有统计学意义(P<0.01)。结论:PPARγ通过下调NF-κB信号通路抑制脂多糖刺激下牙周膜细胞炎症因子RNA表达和蛋白分泌,进而调节牙周炎症反应。

关键词: PPARγ, 罗格列酮, 牙周膜细胞, 炎症因子, NF-κB信号通路

Abstract: Objective: To explore the mechanism of PPARγ in periodontitis. Methods: Human periodontal ligament cells (hPDLCs) were cultured in tissue blocks. Cells were divided into four groups. Group A: normal control group; Group B:LPS group; Group C: rosiglitazone control group; Group D: rosiglitazone group. Expression of PPARγ and NF-κB p65 were detected by western blot. Cell immunofluorescence was employed to determine the location of NF-κB p65 in hPDLCs. RNA expression of IL-1β and TNF-α was detected by realtime PCR and protein expression was detected by ELISA. Results: After stimulated by LPS, protein expression of PPARγ decreased and NF-κB p65 increased in cellular nuclei. Moreover, the RNA and protein expression of IL-1β and TNF-α were significantly increased. When stimulated by LPS and rosiglitazone, protein expression of PPARγ increased and NF-κB p65 decreased in cellular nuclei, and the RNA and protein expression of IL-1β and TNF-α significantly decreased.These difference were statistically significant (P<0.01). Conclusion: PPARγ inhibits lipopolysaccharide-induced RNA expression and protein secretion of cytokines in human periodontal ligament cells via downregulation of NF-κB signaling pathway, and then regulate inflammatory responses in periodontal disease.

Key words: PPARγ, Rosiglitazone , Periodontal ligament cells, Cytokines , NF- κB signaling pathway

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