Department of Stomatology, School of Stomatology of Qingdao University, Qingdao, 266003, Shandong Province, China.
Qingdao Stomatological Hospital Affiliated to Qingdao University, No.17 Dexian Road, Shinan District, Qingdao, 266001, Shandong Province, China.
Inflammation. 2021 Oct;44(5):1843-1855. doi: 10.1007/s10753-021-01462-7. Epub 2021 Apr 11.
To study the effects of psoralen on the intestinal barrier and alveolar bone loss (ABL) in rats with chronic periodontitis. Fifty-two 8-week-old specific pathogen-free (SPF) male Sprague-Dawley (SD) rats were randomly divided into the following four groups: Control group (Control), psoralen group of healthy rats (Pso), periodontitis model group (Model), and psoralen group of periodontitis rats (Peri+Pso). The alveolar bone resorption of maxillary molars was observed via haematoxylin-eosin staining and micro-computed tomography. The expression level of receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG) in periodontal tissues was evaluated by immunofluorescence staining. The changes in serum tumour necrosis factor (TNF)-α, interleukin (IL)-10, IL-6, intestinal mucosal occludin, and claudin-5 were detected using enzyme-linked immunosorbent assay (ELISA). The level of intestinal mucosal NOD2 was detected using immunohistochemical methods. DNA was extracted from the intestinal contents and the 16s rRNA gene was sequenced using an Illumina MiSeq platform. The expression of NOD2 protein in the intestinal tract of periodontitis rats decreased after intragastric psoralen administration. Psoralen increased the intestinal microbiota diversity of rats. The level of serum pro-inflammatory factor TNF-α decreased and the level of anti-inflammatory factor IL-10 increased. ABL was observed to be significantly decreased in rats treated with psoralen. Psoralen decreased the RANKL/OPG ratio of periodontitis rats. Psoralen may affect the intestinal immune barrier and ecological barrier, mediate immune response, promote the secretion of anti-inflammatory factor IL-10, and reduce the secretion of the pro-inflammatory factor TNF-α, thus reducing ABL in experimental periodontitis in rats.
研究补骨脂素对慢性牙周炎大鼠肠道屏障和牙槽骨丢失(ABL)的影响。将 52 只 8 周龄无特定病原体(SPF)雄性 Sprague-Dawley(SD)大鼠随机分为以下四组:对照组(Control)、健康大鼠补骨脂素组(Pso)、牙周炎模型组(Model)和牙周炎大鼠补骨脂素组(Peri+Pso)。通过苏木精-伊红染色和微计算机断层扫描观察上颌磨牙牙槽骨吸收情况。免疫荧光染色评估牙周组织中核因子-κB 受体激活剂配体(RANKL)和骨保护素(OPG)的表达水平。采用酶联免疫吸附试验(ELISA)检测血清肿瘤坏死因子(TNF)-α、白细胞介素(IL)-10、IL-6、肠黏膜闭合蛋白和 Claudin-5 的变化。采用免疫组织化学方法检测肠黏膜 NOD2 水平。从肠内容物中提取 DNA,采用 Illumina MiSeq 平台对 16s rRNA 基因进行测序。灌胃补骨脂素后,牙周炎大鼠肠道 NOD2 蛋白表达减少。补骨脂素增加了大鼠肠道微生物区系的多样性。血清促炎因子 TNF-α水平降低,抗炎因子 IL-10 水平升高。补骨脂素治疗大鼠 ABL 明显减少。补骨脂素降低了牙周炎大鼠的 RANKL/OPG 比值。补骨脂素可能通过影响肠道免疫屏障和生态屏障,调节免疫反应,促进抗炎因子 IL-10 的分泌,减少促炎因子 TNF-α的分泌,从而减少实验性牙周炎大鼠的 ABL。