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作 者:潘旭强 韩靓 石铁军 Pan Xuqiang;Han Liang;Shi Tiejun(Ningbo No.2 Hospital,Ningbo 315010,Zhejiang,China;School/Hospital of Stomatology,Lanzhou University,Lanzhou 730000,China)
机构地区:[1]宁波市第二医院,浙江宁波315010 [2]兰州大学口腔医学院,甘肃兰州730000
出 处:《生物医学转化》2023年第3期80-85,96,共7页Biomedical transformation
摘 要:目的 三叉神经痛是最常见的颌面疼痛综合征,其病因尚未完全明确。本文主要研究G蛋白门控内向整流钾离子通道(G Protein-gated Inwardly Rectifying Potassium Channel,GIRK)蛋白在三叉神经痛中的作用及表达情况,为三叉神经痛的治疗提供新方向。方法 通过眶下神经横断手术建立小鼠的三叉神经痛动物模型,利用Von Frey测量其机械性异常性疼痛;记录其面部抓挠次数来测量其自发痛;使用Western Blot检测三叉神经节中GIRK蛋白的表达情况。结果 研究发现,小鼠三叉神经损伤后,与对照组相比,其机械性异常性疼痛和自发痛在术后3-21天均有显著性增强,而三叉神经节中GIRK1-3蛋白水平均下调。结论 本研究成功建立了小鼠的三叉神经痛模型,表明GIRK可能在神经损伤后的三叉神经痛中发挥重要作用。Objective Trigeminal neuralgia is the most common maxillofacial pain syndrome,and its etiology has not been fully understood.In this paper,we focus on the role and expression of G protein-gated inwardly rectifying potassium channel(GIRK)protein in trigeminal neuralgia to provide a new direction for the treatment of trigeminal neuralgia.Methods An animal model of trigeminal neuralgia in mice was established by infraorbital nerve transection surgery,and its mechanical abnormal pain was measured by using Von Frey;the number of facial scratches was recorded to measure its spontaneous pain;the expression of GIRK protein in trigeminal ganglion was detected by Western Blot.Results Our research discovered that after trigeminal nerve injury in mice,both mechanical abnormal pain and spontaneous pain were significantly enhanced at 3-21 days postoperatively compared to controls,while both GIRK1-3 protein levels were downregulated in the trigeminal ganglion. Conclusion Trigeminal neuralgia model in mice was successfully established, and suggesting thatGIRK may play a significant role in trigeminal neuralgia after nerve injury.
关 键 词:三叉神经痛 G蛋白门控内向整流钾离子通道 机械性异常性疼痛 自发痛
分 类 号:R745.11[医药卫生—神经病学与精神病学]
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