实验性牙周炎细胞因子谱指标的动态变化

Zakhvatov A.N., Khaidar D.A., Tarasova T.V., Begoulov I.V., Z. I.A., Tambovtsev S.A., Parshina A.Yu.
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引用次数: 1

摘要

摘要在研究疾病发病机制的背景下,生理过程的分子水平是疾病诊断和治疗的基础。因此,牙周炎发病机制的特点是促炎细胞因子直接参与替代性炎症的发展。细胞因子谱的研究对诊断和治疗都有意义,因为炎症介质指标的动态反映了牙周炎中存在的病理反应的活性程度和特异性。研究目的:研究实验性牙周炎细胞因子谱指标。材料和方法。在体重190 ~ 280 g的50只非线性白色大鼠的实验中,复制了Shkolnaya K.D, Atrushkevich V.G.提出的实验性牙周炎模型。(专利号:2625295,日期:2017年12月7日)。采用“Bender MedSystems”试剂盒,采用酶联免疫吸附法检测促炎(IL-1β、TNF、IL-6、IL-17)、抗炎(IL-4、IL-10)和调节(IL-2)细胞因子水平,评估血清细胞因子状态的动态变化。结果。该研究揭示了细胞因子系统中存在不平衡,其特征是促炎细胞因子和抗炎细胞因子之间的生理平衡被破坏,并以前者为主。在整个实验过程中,细胞因子的大量产生持续存在,到第25天,上述解偶联增加,这表明牙周组织中形成了免疫炎症过程。结论。本研究获得的数据证实了细胞因子网络失衡的存在,这表明牙周复合体炎症过程的形成和进展,也需要在复合体治疗中引入抑制促炎介质合成的药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
DYNAMICS OF CYTOKINE PROFILE INDICATORS IN EXPERIMENTAL PERIODONTITIS
Abstract. The molecular level of physiological processes in the context of studying the pathogenesis of diseases is the basis for their diagnosis and treatment. Thus, the features of the pathogenesis of periodontitis are the direct participation of pro-inflammatory cytokines in the development of alterative inflammation. The study of the cytokine profile is relevant for both diagnostic and therapeutic purposes, since the dynamics of indicators of inflammatory mediators reflects the degree of activity and specificity of pathological reactions present in periodontitis. The purpose of the study Study of cytokine profile indicators in experimental periodontitis. Materials and methods. In an experiment on 50 white non-linear rats weighing 190-280 g, the model of experimental periodontitis proposed by Shkolnaya K.D., Atrushkevich V.G. was reproduced. (Patent RU No. 2625295 dated 07/12/2017). Assessment of the dynamics of the cytokine status of blood serum was carried out by the level of pro-inflammatory (IL-1β, TNF, IL-6, IL-17), anti-inflammatory (IL-4, IL-10) and regulatory (IL-2) cytokines using enzyme-linked immunosorbent assay using reagent kit "Bender MedSystems". Results. The study revealed the presence of an imbalance in the cytokine system, characterized by a violation of the physiological balance between pro-inflammatory and anti-inflammatory cytokines with a predominance of the former. Hyperproduction of cytokines persisted throughout the experiment with an increase in the above uncoupling by day 25, which indicates the formation of an immunoinflammatory process in the periodontium. Conclusion. The data obtained during the study confirm the presence of an imbalance of the cytokine network, which indicates the formation and progression of the inflammatory process of the periodontal complex, and also necessitates the introduction of drugs that inhibit the synthesis of pro-inflammatory mediators into complex therapy.
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