牙髓炎
三叉神经节
H&E染色
免疫组织化学
医学
牙髓(牙)
炎症
染色
成牙本质细胞
病理
巨噬细胞极化
神经节
化学
巨噬细胞
内科学
解剖
感觉系统
生物
体外
神经科学
生物化学
作者
Lu Gao,Fan Fan,Lina Wang,Bohan Tang,Zhihao Wen,Jing Tang,Ting Dai,Haiwei Jin
摘要
Abstract Background Dental pulp tissues are rich in pain‐related afferent nerve fibers, which originate from primary sensory neurons in the trigeminal ganglion (TG). The mechanisms of central nervous system (CNS) underlying ectopic pain following peripheral inflammation have been reported that the macrophages as inflammatory and immunologic mediators in the TG play an important role in the process of pulpitis and hyperalgesia. Objective(s) To observe the polarization response and dynamic distribution of macrophages in the TG during the development of dental pulp inflammation. Methods A rat model of pulpitis was established using complete Freund's adjuvant (CFA). Hematoxylin‐eosin (HE), immunohistochemistry (IHC), immunofluorescence (IF), toluidine blue (TB) staining, and RT‐qPCR were performed to observe the expression of macrophage‐related factors in the TG. Results The results of IHC staining showed that M2 macrophages labeled with CD206 were observed in the TG of both the control and CFA groups. The statistical analysis indicated that the number of CD206‐positive macrophages in the TG increased significantly at 24 h after CFA‐induced pulpitis, reached a peak at 2 weeks, and then returned to the normal level after 6 weeks. The ratio of M2/M1 in the CFA groups was significantly lower than that in the control group from 24 to 72 h, and this pattern was reversed at 2 weeks after CFA‐induced pulpitis; then, the ratio increased significantly and was maintained at a high level for 4 weeks. RT‐qPCR results showed that the expression of IL‐10 in the TG increased significantly from 1 to 4 weeks after CFA‐induced pulpitis. Conclusion The trend of M2 macrophages was opposite to that of M1 macrophages in the TG during the process of pulpitis induced by CFA, which is consistent with the expression of macrophage‐related cytokines. Macrophage polarization in the TG may participate in the neuroinflammation response induced by dental pulpitis.
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