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首页> 外文期刊>Odontology >Oxidative stress induced by Porphyromonas gingivalis lysate and nicotine in human periodontal ligament fibroblasts
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Oxidative stress induced by Porphyromonas gingivalis lysate and nicotine in human periodontal ligament fibroblasts

机译：Porphyromonas Gingivalis裂解物和尼古丁诱导的氧化应激在人牙周韧带成纤维细胞中

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摘要

Porphyromonas gingivalis (P. gingivalis) and nicotine have been implicated as a major pathogen in the development and progression of periodontitis. One of the possible mechanism is via the oxidative stress of human periodontal ligament fibroblasts (PDLF) which lead to the damage of cell viability and function. This study aimed to investigate oxidative stress (OS) levels in the cultured media of human PDLF under the induction of P. gingivalis lysate and nicotine. Primary PDLF was cultured in growth media under P. gingivalis or/and nicotine treatment in different concentrations for 2 and 24h. Following incubation, oxidative stress molecules malondialdehyde (MDA) and oxidized guanine species (Ox-GS) from the cell cultured supernatant were determined by spectrophotometric assay and ELISA, respectively. DCFDA and superoxide assays were performed to verify the production of ROS and intracellular superoxide radical under various stimuli. As a result, at both 2 and 24h, Ox-GS and MDA levels in the medium of cells treated with different concentrations of P. gingivalis lysate and nicotine, either separately or in combination, were significantly different from the negative controls in a dose- and time-dependent manner. Interestingly, except MDA levels in P. gingivalis lysate at 20 mu g/ml, MDA levels in all other tested conditions were found as same as one in the positive controls after 24h. ROS and superoxide production were enhanced under P. gingivalis and/or nicotine stimulation. Therefore, OS biomarkers were generated by PDLF upon treatment with periodontal pathogens and nicotine which could elucidate a potential local mechanism of periodontal disease etiology via superoxide mediation.
机译：Porphyromonas Gingivalis（P.Gingivalis）和尼古丁被牵连作为牙周炎的发育和进展中的主要病原体。其中一种可能的机制是通过人牙周韧带成纤维细胞（PDLF）的氧化应激，这导致细胞活力和功能的损伤。该研究旨在在诱导P.Gingivalis裂解物和尼古丁的诱导下研究人PDLF培养介质中的氧化应激（OS）水平。在不同浓度的P.Gingivalis或/和尼古丁处理下，在生长培养基中培养初级PDLF，其不同浓度为2和24h。在孵育后，通过分光光度法测定和ELISA测定来自细胞培养上清液的氧化应激分子丙二醛（MDA）和氧化的鸟嘌呤种（OX-GS）。进行DCFDA和超氧化物测定以在各种刺激下验证ROS和细胞内超氧化物的产生。结果，在用不同浓度的P.Gingivalis裂解物和单独或组合的不同浓度的P.Gingivalis裂解物和尼古丁治疗的细胞中的培养基中的Ox-GS和MDA水平与剂量中的阴性对照显着不同和时间依赖的方式。有趣的是，除了在20μg/ ml的P.Gingivalis裂解物中的MDA水平，在24小时后发现所有其他测试条件的MDA水平与阳性对照中的一个相同。在P.Gingivalis和/或尼古丁刺激下提高了ROS和超氧化物产生。因此，在用牙周病原体和尼古丁治疗后，通过PDLF产生OS生物标志物，其可以通过超氧化物调解阐明牙周病病因的潜在局部机制。

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