摘要
目的:研究LPS对人牙周膜成纤维细胞中骨唾液蛋白和白细胞介素-8表达的影响及其相关机制的研究。方法:采用不同浓度LPS处理人牙周膜成纤维细胞(hPDLFs)不同时间,用Real time PCR检测骨唾液酸蛋白和IL-8 mRNA的表达。然后用siTLR2或siTLR4(20 nM)转染hPDLFs或用MAPK信号通路抑制剂抑制hPDLFs,然后用Real time PCR检测骨涎蛋白和IL-8 mRNA和蛋白的表达。结果:0.1 mg/L的LPS处理8 h,显著上调骨唾液蛋白mRNA的表达,而10和50 mg/L的LPS则显著减少骨唾液酸蛋白mRNA的表达。然而,10mg/L的LPS刺激显着增加IL-8 mRNA水平。用si RNA敲除TLR2则完全废除了LPS对骨唾液蛋白m RNA水平的作用对IL-8 mRNA水平的作用。结论:在人类牙周膜成纤维细胞中,LPS通过TLR2信号通路分别抑制骨唾液蛋白和增强IL-8基因的表达。
Objective This study was to research the effect of LPS on the expression of bone sialoprotein and interleukin-8 in human periodontal ligament fibroblasts.Methods The hPDLFs were treated with LPS with different concentrations and then bone sialoprotein and IL-8 mRNA expression were detected using qPCR.Then hPDLFs were transiently transfected with siTLR2 and then bone sialoprotein and IL-8 m RNA were also detected using qPCR.Results Treatments with 0.1 mg/L of LPS for 8 h up-regulated bone sialoprotein mRNA expression,whereas 10 and 50 mg/L of LPS induced a significant decrease in the expression of bone sialoprotein mRNA.In contrast,IL8 mRNA levels were increased significantly by 10 mg/L LPS.Knocking down of the TLR2 by si RNA blocked the effect of LPS on bone sialoprotein and IL-8 in hPDLFs.Conclusion The study demonstrated that in hPDLFs,LPS suppresses bone sialoprotein and enhances IL-8 gene and protein expression via TLR2 signaling pathway.
作者
武月霞
司姗姗
张昕
连克乾
Wu Yue-xia;Si Shan-shan;Zhang Xin;Lian Ke-qian(Department of Orthodontics,Panyu Branch of Stomatological Hospital,Southern Medical University,Guangzhou 511400,China;Department of Stomatology,The First Affiliated Hospital,Sun Yat-sen University,Guangzhou 510080,China;Department of Endodontics,Panyu Branch of Stomatological Hospital,Southern Medical University,Guangzhou 511400,China;Department of Implantology and Prosthodontics,Panyu Branch of Stomatological Hospital,Southern Medical University,Guangzhou 511400,China)
出处
《湖南师范大学学报（医学版）》
2020年第1期77-80,共4页
Journal of Hunan Normal University(Medical Sciences)
作者简介
通讯作者:连克乾,E-mail:wuyuexia126@126.com
