College of Stomatology, Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing, China; Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing, China.
College of Stomatology, Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing, China.
Arch Oral Biol. 2022 Nov;143:105530. doi: 10.1016/j.archoralbio.2022.105530. Epub 2022 Aug 27.
Acute pulpitis is one of the common causes of tooth pain. TACAN (Tmem120a) is a newly identified ion channel that senses mechanical pain. In this experiment, we studied the expression of the TACAN ion channel in the trigeminal ganglia in a rat model of pulpitis to explore the correlation between the expression of this ion channel and inflammatory pain.
Lipopolysaccharide was used to induce acute pulpitis in rats, and pulpitis was assessed histologically. The facial pain threshold of the rats was measured by the von Frey test. TACAN mRNA expression in rat dental pulp and the trigeminal nerve was measured by qPCR, and TACAN protein expression in the trigeminal ganglia was evaluated by western blot analysis and immunofluorescence. Antisense oligonucleotides were used to reduce TACAN protein expression in the trigeminal ganglia, and the change in the pain threshold in the rats with acute pulpitis was determined.
The results showed that the TACAN transcript level in rat pulp tissue increased under inflammatory conditions, and we proved that pulpitis increased TACAN protein expression in the rat ipsilateral trigeminal ganglia. The facial pain threshold was decreased in rats with pulpitis. A short-term decrease in TACAN protein expression could improve the pain threshold.
With the development of pulpitis after bacterial infection, the upregulation of TACAN expression in the trigeminal ganglia promoted pain sensitivity. A short-term reduction in TACAN expression relieved pain. Therefore, this study indicated that TACAN is a potential target channel for new analgesics.
急性牙髓炎是引起牙痛的常见原因之一。TACAN（Tmem120a）是一种新发现的离子通道，可感知机械性疼痛。本实验研究了 TACAN 离子通道在牙髓炎大鼠三叉神经节中的表达，以探讨该离子通道的表达与炎症性疼痛的相关性。
采用脂多糖诱导大鼠急性牙髓炎，并进行组织学评估。通过 von Frey 试验测量大鼠面部疼痛阈值。采用 qPCR 检测大鼠牙髓和三叉神经中 TACAN mRNA 的表达，采用 Western blot 分析和免疫荧光法评估三叉神经节中 TACAN 蛋白的表达。用反义寡核苷酸降低三叉神经节中的 TACAN 蛋白表达，观察急性牙髓炎大鼠疼痛阈值的变化。
结果显示，在炎症条件下，大鼠牙髓组织中的 TACAN 转录本水平增加，我们证明了牙髓炎增加了大鼠同侧三叉神经节中的 TACAN 蛋白表达。牙髓炎大鼠面部疼痛阈值降低。TACAN 蛋白表达的短期降低可提高疼痛阈值。
细菌感染后牙髓炎的发展过程中，三叉神经节中 TACAN 表达的上调促进了痛觉敏感性。TACAN 表达的短期降低可缓解疼痛。因此，本研究表明 TACAN 是一种新的潜在镇痛靶点。
