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机构地区:[1]安徽医科大学口腔医学院口腔预防教研室,合肥230032
出 处:《中华口腔医学杂志》2012年第3期177-181,共5页Chinese Journal of Stomatology
基 金:安徽省科技计划(08020303072)
摘 要:目的 通过检测河豚毒素不敏感型电压门控钠离子通道Nav1.8在正常和疼痛人牙髓组织中表达的变化,探讨Nav1.8与牙痛的关系.方法 选择23颗健康第三磨牙为正常组,24颗伴有自发痛、夜间痛或冷热刺激痛的龋源性牙髓炎第三磨牙为疼痛组,分别采用免疫组织化学法、蛋白质印迹法和反转录聚合酶链法检测并比较正常与炎症人牙髓组织中Nav1.8的表达.结果 在人牙髓组织成牙本质细胞下层Nav1.8呈阳性表达;与正常牙髓组织相比,炎症诱发的疼痛牙髓组织中Nav1.8的表达显著增强;免疫组化结果显示炎症牙髓组织中Nav1.8相对表达强度为0.547±0.049,正常组为0.356±0.058,两组差异有统计学意义(P<0.05);蛋白质印迹法灰度扫描显示疼痛组Nav1.8相对表达量为0.234±0.030,正常组为0.108±0.012,两组差异有统计学意义(P<0.05);定量反转录聚合酶链结果显示疼痛组Nav1.8 mRNA相对表达量(7.130±2.471)较正常组(1.024±0.295)显著提高(P<0.05).结论 在炎症诱发的疼痛牙髓组织中Nav1.8高表达;Nav1.8可能参与了牙髓炎疼痛感觉的发生过程.Objective To investigate the relationship between dental pain and Nav1.8 expression level by detecting the expression of voltage-gated sodium channel Nav1.8 in normal human dental pulps and painful pulp tissues. Methods Immunohistochemistry,reverse transcription polymerase chain reaction (RT-PCR) and Western blotting were used to detect the expression of Nav1.8 in normal human dental pulp and painful dental pulp. Results Nav1.8 expressed in dental pulps and the expression level of Nav1.8 increased significantly in painful dental pulps in comparison with normal dental tissues. The immunohistochemistry results revealed that Nav1.8 expression level in painful dental issue was 0.547 ± 0.049 in relative intensity,and in normal dental issue 0.356 ± 0.058 (P 〈 0.05 ).Western blotting showed similar results of 0.234 ± 0.030 vs 0.108 ± 0.012.RT-PCR results indicated that Nav1.8 mRNA expression level in painful dental issue was 7.130 ± 2.471 and in normal dental issue was 1.024 ± 0.295 ( P 〈 0.05 ).Conclusions The expression level of Nav1.8 increased significantly in painful dental pulp tissue,suggesting that Nav1.8 may play an important role in the development and transmission of dental pain.
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