摘要
目的通过检测大鼠实验性牙髓炎牙髓中电压门控钠离子通道Nav1.7的表达,探讨Nav1.7的表达与牙痛的关系。方法大鼠切牙髓腔暴露,置入脂多糖(LPS)诱导产生牙髓炎。大鼠分为正常对照组和封LPS 1、3、5 d组,HE染色观察各组牙髓组织病理学改变。通过免疫组化、ELISA和逆转录PCR(RT-PCR)方法检测大鼠正常牙髓和炎症牙髓中Nav1.7的表达。结果封LPS 1 d组,牙髓中未见明显炎症,而封LPS 3和5 d组牙髓中炎症反应程度逐渐上升。免疫组化结果显示,Nav1.7在所有牙髓中均有表达,封LPS 3和5 d组牙髓中Nav1.7表达量较正常对照组明显增加(P<0.05);ELISA结果与上述结果相似。RT-PCR结果显示,封LPS 3和5 d组牙髓中Nav1.7 mRNA较正常对照组有显著上调(P<0.05)。结论在牙髓炎中,Nav1.7可能以时序控制方式表达明显增多,且与牙髓炎炎症程度相关。鉴于Nav1.7在疼痛中发挥了重要作用,牙髓中Nav1.7的表达可能涉及牙痛的病理生理机制。
Objective To determine the expression level relationship between dental pain and Nav l. 7 expression of Nail. 7 in inflamed pulps of rats, and to investigate the level. Methods Inflammation was induced by creating pulp exposures to LPS in rat incisors. Histopathological changes in the induced pulpitis were evaluated 1,3, 5 days after exposure. Using immunohistochemistry, reverse transcription polymerase chain reaction （RT-PCR） and En- zyme-linked immunosorbent assay to determine the expression of Navl. 7 in normal pulps and inflamed pulps of rats. Results At day 1, no inflammation was evident in the pulp tissue, whereas increased levels of inflammatory responses were identified at day 3 and day 5. The immunohistochemistry results revealed that Nav 1.7 was expressed in all rat dental pulp and increased significantly at day 3 and day 5 after treatment compared with control group （P 〈0.05）. And ELISA showed similar results. RT-PCR results also demonstrated that Nav1.7 mRNA up-regulated significantly at day 3 and day 5 after treatment compared with normal group （ P 〈 0. 05 ）. Conclusion Nav1. 7 channels seem to be expressed significantly more under a temporal control so as to be inflammation during pulp may contribute pulpitis. As Nay1.7 has been considered to play a role in pain, to thepathophysiology of tooth pain. associated with a severity of its expression within dental
出处
《安徽医科大学学报》
CAS
北大核心
2013年第8期873-877,共5页
Acta Universitatis Medicinalis Anhui
基金
安徽省科技计划项目(编号:12070403063)
