摘要
目的探讨牙龈屏障定居的M1型巨噬细胞在牙周炎发生中的作用以及可能的机制。方法利用随机数字表将36只3月龄的Wistar雌性大鼠按随机数表法分为正常组(C1)、牙周炎模型组(P1)和牙周炎+治疗组(P2)。大鼠牙周炎模型采用去势与结扎相结合的方法。流式细胞术分析牙龈组织中M1型巨噬细胞的比例,以F4/80和CD11c作为M1型巨噬细胞的表面标志物;酶联免疫吸附试验法(ELASA)检测M1型巨噬细胞相关的促炎因子白细胞介素(IL)-1β、IL-6和肿瘤坏死因子(TNF)-α的表达情况。结果成功诱导大鼠牙周炎模型;P1组与C1组相比,M1型巨噬细胞的比例明显上调(P<0.01),IL-1β、IL-6和TNF-α促炎因子的表达明显上调(P<0.01);P2组比P1组M1型巨噬细胞的比例显著下降(P<0.01),IL-1β、IL-6和TNF-α促炎因子的表达显著下降(P<0.01)。结论牙龈定居的M1型巨噬细胞可能通过分泌IL-1β、IL-6和TNF-α促炎因子的表达以及自身比例的增加促进牙周炎的发生。
Objective To investigate the role of M1 macrophages resident in gingival barrier in the development of periodontitis and its possible mechanism.Methods Thirty-six 3-month-old Wistar female rats were randomly divided into normal group(C1 group),periodontitis model group(P1 group)and periodontitis+treatment group(P2 group)using random number table.The rat periodontitis was modeled via a combination of castration and ligation.Flow cytometry was used to measure the proportion of M1 macrophages in gingival tissues,with F4/80 and CD11c as the surface markers of M1 macrophages;ELISA was used to detect the expression of M1 macrophage-associated proinflammatory cytokines IL-1β,IL-6 and TNF-α.Results Rat periodontitis was successfully modeled.Compared with C1 group,the P1 group showed significantly higher proportion of M1 macrophages(P<0.01)and up-regulated expression of proinflammatory cytokines including IL-1β,IL-6 and TNF-α(P<0.01).Compared with P1 group,the P2 group showed significantly lower proportion of M1 macrophages(P<0.01)and decreased expression of IL-1β,IL-6 and TNF-α(P<0.01).Conclusion Gingiva-resident M1 macrophages may promote the development of periodontitis via enhancing the expression of proin flammatory cytokines such as IL-1β,IL-6 and TNF-α,and also via increasing their proportion in the gingival tissue.
作者
吴剑豪
冯贻苗
傅潇慧
Wu Jianhao;Feng Yimiao;Fu Xiaohui(Department of Stomatology,Quzhou People′s Hospital,Zhejiang 324000,China)
出处
《中国药物与临床》
CAS
2019年第23期4037-4039,共3页
Chinese Remedies & Clinics
基金
浙江省中医药科技计划(2014ZA069)。
关键词
牙周炎
巨噬细胞
牙龈定居免疫细胞
Periodontitis
Macrophages
Gingiva-resident immune cells