急性牙髓炎能引起剧烈疼痛，严重影响患者身心健康，但其机制尚不清楚。miR-34a是我们利用芯片从急性牙髓炎模型中筛选得到的miRNA之一。预实验结果显示：急性牙髓炎大鼠延髓背角miR-34a 表达升高、SIRT1降低、NF-κB升高； SIRT1是受miR-34a调控的关键分子，可抑制mGluR5和NF-κB表达，在miR-34a调控急性牙髓炎疼痛中发挥了重要作用；过表达mGluR5可增强NF-κB活性、NF-κB活化上调miR-34a表达；以上结果提示miR-34a/SIRT1/mGluR5/NF-κB环路可能参与急性牙髓炎伤害性信息的处理。本课题拟应用分子生物学、形态学和行为学等方法，系统研究miR-34a/SIRT1/mGluR5/NF-κB环路在急性牙髓炎疼痛中枢调控中发挥的作用及其调控机制，为急性牙髓炎疼痛中枢调控机制研究提供新的认识，为临床治疗急性牙髓炎提供潜在的药物作用靶点。

Acute pulpitis can cause violent and unbearable spontaneous pain, severely disturbing patients’ mental and physical health, but the specific central mechanism remains unclear. miR-34a was one of the miRNAs screened by miRNAs differential expression chips from the medullary dorsal horn of rat acute pulpitis model. Our preliminary experiments reveal that rat acute pulpitis model was successfully developed with obvious pain behaviors, and significantly increased miR-34a, decreased SIRT1, and up-regulated NF-κB were detected in the medullary dorsal horn. Moreover, SIRT1, as a key target of miR-34a, could inhibit the expression of mGluR5 and NF-κB, and plays a pivotal role in the regulation of nociceptive information by miR-34a under acute pulpitis pain conditions. Furthermore, overexpression of mGluR5 could enhance the activity of NF-κB, while NF-κB activation could upregulate the expression of miR-34a. These results suggest that miR-34a/SIRT1//mGluR5 NF-κB pathway may participate in the regulation of nociceptive information under acute pulpitis pain conditions. In this study, by using experiment techniques in molecular biology, neuropharmacology, morphology and pain behavior, we plan to observe the dynamic changes of miR-34a, SIRT1, mGluR5 and NF-κB in medullary dorsal horn in acute pulpitis pain models and the neuron types involved in this process. Afterwards, we will aim at exploring the effects on acute pulpitis pain by interfering with the function of miR-34a, SIRT1, mGluR5 and NF-κB in the medullary dorsal horn. Furthermore, the molecular mechanism of miR-34a/SIRT1/mGluR5/NF-κB signal pathway in regulation of acute pulpitis pain will be studied. The results will provide new insight into the recognition of central regulation of acute pulpitis pain, and offer potential intervention targets for the development of new pulpitis pain analgesic medications.