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Effects of experimental pulpitis on the expression of transient receptor potential channels on the rat trigeminal ganglia.

机译:实验性牙髓炎对大鼠三叉神经节瞬时受体电位通道表达的影响。

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摘要

Management of patients who present with tooth pain is one of the major challenges in dentistry. Further elucidation of mechanisms underlying tooth pain would lead to optimized management of these patients. Recent evidence suggests that Transient Receptor Potential (TRP) channels participate in pain sensation induced by chemical, thermal and mechanical stimuli. The aim of this study is to explore the molecular mechanisms underlying pulpitis by investigating the involvement of transient receptor potential vanilloid 1 (TRPV1) and transient receptor potential ankyrin 1 (TRPA1) channels in tooth pain using an animal model. Experiments were performed on 42 male Sprague--Dawley rats. Pulpitis was induced by drilling the first maxillary molar of the animal and treating the cavity with either complete Freund's adjuvant (CFA) or saline. Naive (untreated) rats were used as control. Trigeminal ganglia (TG) from both sides were extracted 1, 3 and 7 days after pulpitis induction and Western blot analysis was performed. The data was analyzed with one-way ANOVA or Kruskal-Wallis ANOVA on ranks depending on the outcome of normality test. TG from naive and pulpitis-induced rats showed the expression of both TRPV1 and TRPA1. Increased expression of both receptors was observed in TG of rats treated with saline and CFA, compared to naive (untreated) rats. However, results were not statistically significant due to a large variability. Potential factors that might have contributed to the variability, strengths and limitations of the pulpitis model employed in this study are discussed. Confirmation of our results with larger samples may provide a rationale for targeting these channels and reveal new therapeutic strategies for pulpitis.
机译:出现牙齿疼痛的患者的管理是牙科的主要挑战之一。进一步阐明牙齿疼痛的潜在机制将导致这些患者的最佳治疗。最近的证据表明,瞬态受体电位(TRP)通道参与了由化学,热和机械刺激引起的疼痛感。这项研究的目的是通过使用动物模型调查牙痛中瞬时受体电位香草酸1(TRPV1)和瞬时受体电位锚蛋白1(TRPA1)通道的参与,探讨牙髓炎的分子机制。实验是对42只雄性Sprague-Dawley大鼠进行的。通过在动物的上颌第一磨牙上钻孔并用完全弗氏佐剂(CFA)或生理盐水处理空腔来诱发牙髓炎。幼稚(未治疗)大鼠用作对照。牙髓炎诱导后1、3和7天从两侧提取三叉神经节(TG),并进行蛋白质印迹分析。根据正态性检验的结果,对数据进行单向方差分析或Kruskal-Wallis方差分析。幼稚和牙髓炎诱导的大鼠的TG显示TRPV1和TRPA1的表达。与未处理(未处理)的大鼠相比,在用盐水和CFA处理的大鼠的TG中观察到两种受体的表达均增加。但是,由于差异较大,结果在统计上并不显着。讨论了可能影响本研究中牙髓炎模型的变异性,强度和局限性的潜在因素。用更大的样本证实我们的结果可能为针对这些渠道提供依据,并揭示了牙髓炎的新治疗策略。

著录项

  • 作者

    Duraes, Gabriela Versiani.;

  • 作者单位

    University of Maryland, Baltimore.;

  • 授予单位 University of Maryland, Baltimore.;
  • 学科 Health Sciences Dentistry.
  • 学位 M.S.
  • 年度 2010
  • 页码 59 p.
  • 总页数 59
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 地球物理学;
  • 关键词

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