Background Dexmedetomidine (Dex) is a highly selective agonist of the α2 adrenergic receptor and a common sedative; however, its anti-inflammatory effect has been studied. In this study, the inhibitory effect of Dex on inflammation in dental pulp cells was assessed. For this, the effect of Dex on inflammation induced by carrageenan (Car) in human dental pulp cells (hDPCs) was evaluated. Car incubation induced a robust inflammatory response in hDPCs as well as activation of PKA-STAT3 and PKC-nuclear factor kappa B (NF-κB) signaling pathways. Results Dex reduced the expression of inflammatory cytokines in a dose-dependent manner. Meanwhile, the phosphorylation of PKA, PKC, STAT3, and NF-κB as well as the nuclear accumulation of STAT3 and NF-κB were significantly increased in Dex-treated Car-induced hDPCs. Western blotting results also showed that the phosphorylation level of transient receptor potential cation channel subfamily V member 1 (TRPV1) was downregulated as a result of Dex treatment. Furthermore, we found that administration of the TRPV1 agonist capsaicin (Cap) reversed the effects of Dex on proinflammatory cytokines; however, the expression and activation of PKA-STAT3 and PKC-NF-κB signals were not altered owing to Cap administration. Conclusions These results indicate that Dex plays a defensive role in dental pulp inflammation by regulating the TRPV1 channel and can be used as a potential target for human dental pulp inflammation intervention.

中文翻译：

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由于右美托咪定降低了 TRPV1 活性，抑制了角叉菜胶诱导的牙齿炎症反应。

背景 右美托咪定 (Dex) 是一种高选择性的 α2 肾上腺素受体激动剂，也是一种常见的镇静剂。然而，已经研究了它的抗炎作用。本研究评估了Dex对牙髓细胞炎症的抑制作用。为此，评估了 Dex 对人牙髓细胞 (hDPC) 中角叉菜胶 (Car) 诱导的炎症的影响。汽车孵化在 hDPC 中诱导了强烈的炎症反应，并激活了 PKA-STAT3 和 PKC-核因子 kappa B (NF-κB) 信号通路。结果Dex以剂量依赖性方式降低炎性细胞因子的表达。同时，在 Dex 处理的 Car 诱导的 hDPC 中，PKA、PKC、STAT3 和 NF-κB 的磷酸化以及 STAT3 和 NF-κB 的核积累显着增加。蛋白质印迹结果还表明，Dex 处理导致瞬时受体电位阳离子通道亚家族 V 成员 1 (TRPV1) 的磷酸化水平下调。此外，我们发现施用 TRPV1 激动剂辣椒素 (Cap) 可逆转 Dex 对促炎细胞因子的影响；然而，由于 Cap 给药，PKA-STAT3 和 PKC-NF-κB 信号的表达和激活没有改变。结论 这些结果表明Dex通过调节TRPV1通道在牙髓炎症中发挥防御作用，可作为人类牙髓炎症干预的潜在靶点。我们发现施用 TRPV1 激动剂辣椒素 (Cap) 可逆转 Dex 对促炎细胞因子的影响；然而，由于 Cap 给药，PKA-STAT3 和 PKC-NF-κB 信号的表达和激活没有改变。结论 这些结果表明Dex通过调节TRPV1通道在牙髓炎症中发挥防御作用，可作为人类牙髓炎症干预的潜在靶点。我们发现施用 TRPV1 激动剂辣椒素 (Cap) 可逆转 Dex 对促炎细胞因子的影响；然而，由于 Cap 给药，PKA-STAT3 和 PKC-NF-κB 信号的表达和激活没有改变。结论 这些结果表明Dex通过调节TRPV1通道在牙髓炎症中发挥防御作用，可作为人类牙髓炎症干预的潜在靶点。