Expression and characterization of vanilloid receptor subtype 1 in human dental pulp cell cultures.

我们检测了人牙髓成纤维细胞（PF-10）是否具有香草样素受体亚型1（VR1）及其与白细胞介素(IL)-6表达的关系。RT-PCR、Western blotting和免疫细胞化学分析结果显示VR1在PF-10细胞上表达。ELISA结果显示，VR1拮抗剂辣椒素可抑制辣椒素诱导的与牙髓炎症有关的IL-6的产生。此外，我们还研究了丝裂原活化蛋白激酶（MAPKs）在辣椒素诱导IL-6产生中的活性。辣椒素刺激后，检测p38 MAPK和c-Jun nh_2末端激酶（JNK）的磷酸化。p38 MAPK参与辣椒素诱导的IL-6的产生，如使用该激酶的特异性抑制剂所示。EMSA结果显示，辣椒素抑制肿瘤坏死因子α (TNF-α)诱导的核因子κB （NF-κB）活化。这些结果提示VR1的激活可能在牙髓炎症中起重要作用。

We examined whether human dental pulp fibroblasts(PF-10) have vanilloid receptor subtype 1(VR1) and its relationship with interleukin(IL)-6 expressions. Results of RT-PCR, Western blotting and immunocytochemical analysis indicate VR1 expression on PF-10 cells. As shown by ELISA, VR1 antagonist, capsazepine inhibited capsaicin-induced IL-6 production which is implicated in pulp inflammation. Furthermore, we investigated the activities of mitogen-activated protein kinases(MAPKs) in capsaicin induced IL-6 production. The phosphorylation of p38 MAPK and c-Jun NH_2-terminal kinase(JNK) were detected after capsaicin stimulation. p38 MAPK is involved in capsaicin-induced IL-6 production, as shown by the use of specific inhibitors of this kinase. The result of EMSA showed capsaicin inhibited tumor necrosis factor-alpha(TNF-α)-induced nuclear factor-kappa B(NF-κB) activations. These results suggest that the activation of VR1 may play an important role in dental pulp inflammation.