Bodet Charles, La Vu Dang, Gafner Stefan, Bergeron Chantal, Grenier Daniel
Research Group in Oral Ecology, Faculty of Dentistry, Laval University, Quebec City, Quebec, Canada.
J Periodontol. 2008 Sep;79(9):1752-61. doi: 10.1902/jop.2008.080052.
Periodontal diseases are a group of inflammatory disorders initiated by specific Gram-negative periodontopathogenic bacteria that lead to the destruction of tooth-supporting tissues. In this study, we tested whether a carbon dioxide-supercritical extract of Glycyrrhiza uralensis (licorice) can reduce the periodontopathogen-induced inflammatory response.
Monocyte-derived macrophages were treated with various concentrations of the licorice extract prior to being stimulated with Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) and Porphyromonas gingivalis lipopolysaccharide (LPS). The capacity of the licorice extract to mediate the inflammatory response was also tested in an ex vivo whole blood model stimulated with P. gingivalis LPS. The secretion of interleukin (IL)-1beta, -6, and -8 and tumor necrosis factor-alpha (TNF-alpha) in both models was assessed by enzyme-linked immunosorbent assays. Changes in the phosphorylation state of macrophage intracellular kinases induced by A. actinomycetemcomitans LPS and the licorice extract in the macrophage model were characterized by immunoblotting.
The licorice extract exhibited potent anti-inflammatory properties, inhibiting the periodontopathogen LPS-induced IL-1beta, -6, and -8 and TNF-alpha responses of macrophages. The licorice extract inhibited the phosphorylation of important macrophage intracellular signaling proteins, including nuclear factor-kappa B p65 nuclear transcription factor and Jun proto-oncogene-encoded activator protein (AP) 1 transcription factor, which are involved in inflammatory signaling pathways. The licorice extract was also a potent inhibitor of the proinflammatory cytokine response in the ex vivo human whole blood model.
This CO(2)-supercritical licorice extract is a potential candidate for the development of a new therapy to prevent and/or treat periodontitis-associated tissue destruction.
牙周疾病是一组由特定革兰氏阴性牙周病原菌引发的炎症性疾病，可导致牙齿支持组织的破坏。在本研究中，我们测试了甘草的二氧化碳超临界提取物是否能减轻牙周病原菌诱导的炎症反应。
在单核细胞衍生的巨噬细胞受到伴放线聚集杆菌（以前称为伴放线放线杆菌）和牙龈卟啉单胞菌脂多糖（LPS）刺激之前，用不同浓度的甘草提取物进行处理。还在牙龈卟啉单胞菌LPS刺激的离体全血模型中测试了甘草提取物介导炎症反应的能力。通过酶联免疫吸附测定法评估两种模型中白细胞介素（IL）-1β、-6和-8以及肿瘤坏死因子-α（TNF-α）的分泌情况。通过免疫印迹法表征巨噬细胞模型中伴放线聚集杆菌LPS和甘草提取物诱导的巨噬细胞细胞内激酶磷酸化状态的变化。
甘草提取物具有强大的抗炎特性，可抑制牙周病原菌LPS诱导的巨噬细胞IL-1β、-6、-8和TNF-α反应。甘草提取物抑制了重要的巨噬细胞细胞内信号蛋白的磷酸化，包括参与炎症信号通路的核因子-κB p65核转录因子和原癌基因编码的激活蛋白（AP）1转录因子。甘草提取物也是离体人全血模型中促炎细胞因子反应的有效抑制剂。
这种二氧化碳超临界甘草提取物是开发预防和/或治疗牙周炎相关组织破坏新疗法的潜在候选物。
Zotero 插件