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Signaling pathways associated with the expression of inflammatory mediators activated during the course of two models of experimental periodontitis

机译：与在两种实验牙周炎模型期间激活的炎症介质表达相关的信号传导途径

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Aims: Evaluate the signaling pathways associated with inflammatory mediators activated in two models of experimental periodontitis.Main methods: Two models were used: lipopolysaccharide (IPS) injections and ligature placement. Wistar rats were used and 30 mug LPS from Escherichia coli was injected twice a week into the palatal aspect of the upper molars. Ligatures were placed around lower first molars. A control group received injections of PBS on the palatal gingivae whereas no ligatures were placed on the lower molars. Samples were collected 5,15 and 30 days and processed for analysis by Western blotting and stereometry.Key findings: The ligature model was associated with rapid and transient activation of extracellular-regulated kinases (ERK) and p38 mitogen-activated protein kinase (MAPK) as well as of nuclear factor kappa B (NF-kappaB). Activation of these signaling pathways on the LPS model was delayed but sustained throughout the 30-day experimental period. Inflammatory changes induced by both models were similar; however there was a significant reduction on inflammation degree on the ligature model, which paralleled the decrease observed on the activation of the signaling pathways. Activation of signal transducer and activator of transcription (STAT)-3 by phosphorylation of Tyrosine residues and of STAT-5 was observed only on the ligature model. Significance: Regulation of gene expression results from the activation of signaling pathways initiated by receptor-ligand binding of external antigens and also of cytokines produced by the host immune system. Understanding the signaling pathways relevant for a given condition may provide information useful for novel therapeutic approaches.
机译：目的：评估与实验periodontitis.Main方法的两个模型激活炎症介质相关的信号转导途径：使用两种模型：脂多糖（IPS）注射和结扎线放置。 Wistar大鼠和用来自大肠杆菌的30个LPS每周两次注入上臼齿的腭方面。结扎线周围放置下第一磨牙。而没有结扎线放置在下臼齿对照组接受上腭牙龈的PBS注射。将样品收集5,15和30天，通过Western印迹和stereometry.Key结果分析处理：该结扎模型用细胞外调节激酶（ERK）和p38促分裂原活化蛋白激酶的快速和瞬时激活（MAPK）相关联以及核因子κB的（NF-κB的）。在LPS模型中，这些信号通路的激活被推迟，但在整个30天的实验期间持续。通过这两种模式是相似的诱导炎症改变;然而有上的结扎模型，它平行于所述信号转导途径的活化所观察到的降低的炎症程度显著减少。仅观察到对结扎模型信号转导和转录（STAT）的活化剂-3通过酪氨酸残基的磷酸化和STAT-5的活化。意义：通过从受体 - 配体外部的抗原的被宿主免疫系统产生的细胞因子的结合和还启动信号转导途径的激活基因表达结果的调节。了解信号传导途径相关的给定条件可提供用于新的治疗方法的有用信息。

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