期刊导航

论文摘要

脂多糖对人牙周膜干细胞增殖及炎性因子表达的影响

Effect of lipopolysaccharide on proliferation and inflammatory factors expression of human periodontal liga-ment stem cells

作者:王岚 夏佳佳 刘琪 金岩

Author:Wang Lan, Xia Jiajia, Liu Qi, Jin Yan.

收稿日期:          年卷(期)页码:2013,31(3):286-286-290

期刊名称:华西口腔医学杂志

Journal Name:West China Journal of Stomatology

关键字:脂多糖,人牙周膜干细胞,炎性因子,

Key words:lipopolysaccharide,human periodontal ligament stem cells,inflammatory factor,

基金项目:

国家自然科学基金资助项目(30725042,81020108019);贵州省省长基金资助项目(C_393)

中文摘要

目的 观察牙龈卟啉单胞菌脂多糖(LPS)对人牙周膜干细胞(HPDLSCs)增殖及炎性因子表达的影响。方法 培养和鉴定HPDLSCs。实验分为3组,A组采用含有10 μg•mL-1 LPS的α-MEM培养液培养HPDLSCs,B组采用含有10 ng•mL-1 LPS刺激单核细胞的上清液培养HPDLSCs,C组采用α-MEM培养液培养HPDLSCs。MTT法检测HPDLSCs的增殖能力,逆转录聚合酶链反应(RT-PCR)检测HPDLSCs白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)mRNA的表达。结果 HPDLSCs具有克隆形成能力和骨向及脂向分化能力。与C组相比,A组和B组均抑制HPDLSCs的增殖,且B组比A组的抑制作用更明显(P结论 牙龈卟啉单胞菌可通过LPS直接或间接地一方面抑制HPDLSCs的增殖,另一方面增加炎性因子的表达,从而加重牙周炎症组织的损伤,延缓牙周组织的自我修复。

英文摘要

Objective To investigate the effect of Porphyromonas gingivalis lipopolysaccharide(LPS) on proliferation and inflammatory factors expression of human periodontal ligament stem cells(HPDLSCs).Methods HPDLSCs were cultivated and identified. Experiment was divided into 3 groups according to culture solution: Group A with α-MEM culture solution containing 10 μg•mL-1LPS, group B with supernatant fluid containing 10 ng•mL-1LPS stimulated mono-cyte, group C with α-MEM culture solution. The proliferation ability of HPDLSCs was analyzed by MTT assay. The ex-pression levels of interleukin-1β(IL-1β), interleukin-6(IL-6), tumor necrosis factor(TNF-α) mRNA of HPDLSCs were detected by reverse transcriptase polymerase chain reaction(RT-PCR).Results HPDLSCs had clonality, bone and fat differentiation ability. Compared with group C, the proliferation ability of HPDLSCs of group A and group B was sig-nificantly inhibited, and the proliferation ability of HPDLSCs of group B were more significantly inhibited than that of group A(PConclusion Porphyromonas gingivalis may inhibit the proliferation of HPDLSCs directly or indirectly through LPS and increase expression of inflammatory factor, exacerbate periodontal inflammatory tissue damage and delay the self-repairing of periodontal tissue.

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