Resistin Is Increased in Periodontal Cells and Tissues: In Vitro and In Vivo Studies
Resistin Is Increased in Periodontal Cells and Tissues: In Vitro and In Vivo Studies
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DOI：
10.1155/2020/9817095
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发表时间：
2020-01-20
影响因子：
4.6
通讯作者：
Cirelli, Joni A.
中科院分区：
文献类型：
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作者：
Nogueira, Andressa V. B.;Nokhbehsaim, Marjan;Cirelli, Joni A.
抵抗素是一种促炎性脂肪因子，在许多炎症性疾病中都会升高。然而，人们对其在牙周炎中的表现知之甚少。本研究旨在评估炎症/微生物应激下牙周细胞和组织中抵抗素的表达和合成以及其对牙周组织的影响。在体内，24只雄性大鼠被随机分为两组：对照组和结扎诱导的牙周病组。 6天和12天后，处死动物以分析脂肪因子、骨质流失、炎症和抵抗素合成的基因表达。在体外，使用人牙周膜（PDL）成纤维细胞来评估炎症刺激后抵抗素的表达。此外，将 PDL 成纤维细胞暴露于抵抗素以评估其对软组织和硬组织代谢标志物的作用。牙周炎组表现出明显的骨质流失，炎症细胞和血管结构数量增加，抵抗素表达和合成增加，脂联素、瘦素及其功能受体表达减少。 PDL 成纤维细胞响应 IL-1 β 的炎症刺激，抵抗素表达和合成显着增加。抵抗素诱导 PDL 成纤维细胞中细胞因子表达的增加以及一些硬组织和基质形成基因的调节减少。这些数据表明抵抗素是由牙周细胞和组织产生的，并且这种作用会因炎症刺激而增强。此外，抵抗素似乎通过减少与基质形成和骨组织相关的标记物来干扰牙周炎期间的软组织和硬组织代谢。
Resistin, a proinflammatory adipokine, is elevated in many inflammatory diseases. However, little is known about its performance in periodontitis. The present study is aimed at evaluating resistin expression and synthesis in periodontal cells and tissues under inflammatory/microbial stress in addition to its effects on the periodontium. In vivo, 24 male rats were randomly divided into two groups: control and ligature-induced periodontal disease. After 6 and 12 days, animals were sacrificed to analyze gene expression of adipokines, bone loss, inflammation, and resistin synthesis. In vitro, human periodontal ligament (PDL) fibroblasts were used to evaluate the expression of resistin after inflammatory stimuli. In addition, PDL fibroblasts were exposed to resistin to evaluate its role on soft and hard tissue metabolism markers. The periodontitis group demonstrated significant bone loss, an increase in the number of inflammatory cells and vascular structures, an increase in resistin expression and synthesis, and a decrease in the expression of adiponectin, leptin, and its functional receptor. PDL fibroblasts showed a significant increase in resistin expression and synthesis in response to the inflammatory stimulus by IL-1 beta. Resistin induced an increase in cytokine expression and a decrease in the regulation of some hard tissue and matrix formation genes in PDL fibroblasts. These data indicate that resistin is produced by periodontal cells and tissues, and this effect is enhanced by inflammatory stimuli. Moreover, resistin seems to interfere with soft and hard tissue metabolism during periodontitis by reducing markers related to matrix formation and bone tissue.