首页> 外文期刊>Journal of Endodontics: Official Journal of American Association of Endodontists >Camphorquinone inhibits odontogenic differentiation of dental pulp cells and triggers release of inflammatory cytokines
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Camphorquinone inhibits odontogenic differentiation of dental pulp cells and triggers release of inflammatory cytokines

机译:樟脑醌抑制牙髓细胞的牙源性分化并触发炎性细胞因子的释放

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Introduction: Camphorquinone (CQ) is a photoinitiator that triggers polymerization of light-curing materials such as dental adhesives and composites. CQ does not become a part of the polymer network, suggesting that CQ can be leached out into surrounding environment including dental pulp and exert adversary effects on tissues. In order to understand the mechanisms of CQ-induced side effects, we investigated the effect of CQ on cell viability, cytokine secretion, and odontogenic differentiation of dental pulp stem cells in vitro. Methods: Cell viability was assessed using the 3-(4,5-dimethylthiazol-2- yl)-2,5-diphenyltetrazolium bromide (MTT) assay after CQ exposure. Western blotting was performed for p16INK4A, p21WAF1, and p53. Secretory cytokines were evaluated using the membrane-enzyme-linked immunosorbent assay as well as conventional and quantitative reverse-transcription polymerase chain reaction. The effects of CQ on odontogenic differentiation were evaluated using alkaline phosphatase and alizarin red S staining methods. Results: CQ treatment suppressed the proliferation of DPSCs and induced the expression of p16INK4A, p21WAF1, and p53. Levels of proinflammatory cytokines (eg, interleukin 6, interleukin 8, and matrix metalloproteinase-3 [MMP3]) were increased by CQ treatment. CQ also inhibited odontogenic differentiation and mineralization capacities of DPSC and MC3T3-E1 cells. Conclusions: Our study showed that CQ may trigger pulpal inflammation by inducing proinflammatory cytokine production from the pulpal cells and may impair odontogenic differentiation of dental pulp cells, resulting in pulpal irritation and inflammation. ? 2013 American Association of Endodontists.
机译:简介:樟脑醌(CQ)是一种光引发剂,可引发光固化材料(例如牙科用粘合剂和复合材料)的聚合。 CQ并未成为聚合物网络的一部分,这表明CQ可以浸出到包括牙髓的周围环境中,并对组织产生不利影响。为了了解CQ诱导的副作用的机制,我们调查了CQ对牙髓干细胞的细胞活力,细胞因子分泌和牙源性分化的影响。方法:在暴露于CQ后,使用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物(MTT)分析评估细胞活力。对p16INK4A,p21WAF1和p53进行了蛋白质印迹。使用膜酶联免疫吸附测定以及常规和定量逆转录聚合酶链反应评估分泌的细胞因子。使用碱性磷酸酶和茜素红S染色方法评估CQ对牙源性分化的影响。结果:CQ处理可抑制DPSC的增殖并诱导p16INK4A,p21WAF1和p53的表达。通过CQ处理,促炎细胞因子(例如白介素6,白介素8和基质金属蛋白酶3 [MMP3])的水平增加。 CQ还抑制了DPSC和MC3T3-E1细胞的牙源性分化和矿化能力。结论:我们的研究表明CQ可能通过诱导牙髓细胞产生促炎性细胞因子来引发牙髓炎症,并可能损害牙髓细胞的牙源性分化,从而导致牙髓刺激和炎症。 ? 2013美国牙医学院会员协会。

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