Topical application of glycyrrhetinic acid in the gingival sulcus inhibits attachment loss in lipopolysaccharide-induced experimental periodontitis in rats
Topical application of glycyrrhetinic acid in the gingival sulcus inhibits attachment loss in lipopolysaccharide-induced experimental periodontitis in rats
复制标题
牙龈沟局部应用甘草次酸可抑制脂多糖诱导的大鼠实验性牙周炎的附着丧失
DOI：
10.1111/jre.12529
复制
发表时间：
2018
影响因子：
3.5
通讯作者：
Hara Y.
中科院分区：
文献类型：
--
作者：
Takamori A.;Yoshinaga Y.;Ukai T.;Nakamura H.;Takamori Y.;Izumi S.;Shiraishi C.;Hara Y.
背景和目的连接上皮附着丧失和牙槽骨破坏是牙周炎的征兆，牙周炎主要是由牙菌斑的炎症反应引起的。甘草次酸 (GA) 是甘草的一种成分，已被证明具有重要的抗炎活性；但此前尚未见其抑制作用预防牙周病的报道。因此，在本研究中，我们利用我们的实验性牙周炎模型，试图评估GA是否对预防附着丧失和牙槽骨丧失有作用。材料与方法用大肠杆菌脂多糖（LPS）腹膜内免疫大鼠。 LPS 组（n = 5）接受 3 次 50 μg/μL LPS 局部涂抹，然后将媒介物（丙二醇：乙醇：磷酸盐缓冲盐水 [PBS] = 8:1:1）涂抹到牙龈沟中。该方案每天重复两次，持续 10 天。低组 (n = 5) 和高组 (n = 5) 分别接受 LPS 和 0.03% 或 0.3% GA 的局部应用。对照组接受局部应用 PBS 和媒介物。第10天将大鼠处死。通过组织计量学研究附着丧失、牙槽骨水平和炎症细胞浸润。免疫组织学评价免疫复合物的形成和LPS的浸润。结果与对照组相比，LPS组的附着丧失、免疫复合物的形成和炎性细胞的浸润增加，而与LPS组相比，低和高组完全被抑制。与对照组和 GA 治疗组相比，LPS 组显示出更大的牙槽骨破坏。此外，在LPS组中检测到LPS的侵袭，在对照组中不存在，并且在GA处理组中比LPS组更弱。结论在本研究中，我们表明GA在大鼠实验性牙周炎模型中抑制牙周破坏。
Background and ObjectiveAttachment loss of the junctional epithelium and alveolar bone destruction are signs of periodontitis, which is mainly caused by an inflammatory response to dental plaque. Glycyrrhetinic acid (GA), a component of the licorice herb, has been shown to have important anti‐inflammatory activities; however, there are no previous reports on the ability of its inhibitory effects to prevent periodontal diseases. Hence, in this study, using our experimental periodontitis model, we attempted to evaluate whether GA had an effect on the prevention of attachment loss and alveolar bone loss.Material and MethodsRats were intraperitoneally immunized withEscherichia colilipopolysaccharide (LPS). The LPS group (n = 5) received 3 topical applications of 50 μg/μL of LPS followed by one application of the vehicle (propylene glycol:ethyl alcohol:phosphate‐buffered saline [PBS] = 8:1:1) into the gingival sulcus. This protocol was repeated twice per day for 10 days. The low (n = 5) and high (n = 5) groups received topical application of LPS and 0.03% or 0.3% GA, respectively. The control group received topical application of PBS and vehicle. The rats were killed on the 10th day. Attachment loss, alveolar bone level and inflammatory cell infiltration were investigated histometrically. The formation of immune complexes and infiltration of LPS were evaluated immunohistologically.ResultsAttachment loss, formation of immune complexes and infiltration of inflammatory cells were increased in the LPS group compared with the control group, and were completely inhibited in the low and high groups compared with the LPS group. The LPS group showed greater alveolar bone destruction compared with the control group and GA‐treated groups. In addition, invasion of LPS was detected in the LPS group, was absent in the control group and was weaker in the GA‐treated groups than in the LPS group.ConclusionIn the present study, we showed that GA inhibits periodontal destruction in the rat experimental periodontitis model.