摘要
目的探讨钠通道亚型Nav1.3的表达与炎性疼痛之间的关系。方法大肠杆菌内毒素(LPS)诱导大鼠牙髓炎后,在伤后1、3、5 d处死。取正常大鼠及牙髓炎大鼠牙髓组织,采用免疫组织化学法检测Nav1.3在牙髓炎牙髓组织的表达;Western blot法检测Nav1.3的蛋白表达情况。结果与正常大鼠牙髓组织相比,诱导牙髓炎后的大鼠牙髓的成牙本质细胞层中Nav1.3表达显著增强,免疫组化结果显示:正常组、实验1、3、5 d组的平均光密度分别为:0.263 1±0.060 9、0.362 8±0.061 0、0.524 9±0.181 5、0.635 4±0.216 0,实验组与对照组相比,差异有统计学意义(P<0.05)。Western blot检测结果显示:正常组、实验1、3、5 d组的Nav1.3蛋白表达量分别为:0.320±0.041、0.551±0.038、0.983±0.027、1.142±0.019,实验组与对照组相比,差异有统计学意义(P<0.05)。结论牙髓炎所致的炎性疼痛可导致Nav1.3蛋白表达显著上调,这可能是炎性疼痛发生时神经元细胞膜上钠通道功能异常的分子学基础之一。
Objective To investigate the relationship between Nav1. 3 expression level and dental pain. Methods The experimental pulpitis model was established in adult male Spragne Dawley rats by using E. coli LPS. The ex- pression of Nav1. 3 in normal dental pulps in rat and painful pulp tissues in rats at 1,3,5 d were measured using immunohistoehemistry and Western blot. Results The expression level of Nav1. 3 increased significantly in painful dental pulps in rats in comparison with normal dental tissues in rats. The immunohistoehemistry results revealed that Nav1. 3 expression level in normal dental issues in rats and painful pulp tissues in rats at 1,3,5 d was 0. 635 4 ±0. 216 0,0. 362 8 ±0. 061 0,0. 524 9 ±0. 181 5,0. 635 4 ±0. 216 0 respectively （P 〈0. 05）. Western blot showed similar results of 0. 320 ±0. 041,0. 551 ±0. 038,0. 983 ±0. 027,1. 142 ±0. 019. Conclusion Pulpitis can cause significant up-regulation of Nav1. 3 protein, which may be related to the molecular mechanism of functional alternation of sodium channels.
出处
《安徽医科大学学报》
CAS
北大核心
2014年第1期32-35,共4页
Acta Universitatis Medicinalis Anhui
基金
安徽省科技厅年度项目(编号:12070403063)
