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药物过度使用的头痛与血流中的高脂多糖糖结合蛋白和促炎分子有关

Hale Gök Dağıdır¹, Elif Topa², Doga Vuralli^1,2,3

¹Neuroscience and Neurotechnology Center of Excellence (NÖROM), Gazi University, Beşevler, Ankara, Türkiye.

The journal of headache and pain

|November 8, 2023

概括

在老鼠中,非类固醇抗炎药物 (NSAID) 诱导的药物过度使用头痛 (MOH) 与肠道泄漏有关. 这项研究发现脂多糖结合蛋白 (LBP) 和炎症标记物水平升高,这表明肠道屏障破坏在MOH中的作用.

科学领域:

神经科学是一个神经科学.
胃肠病学胃肠病学
药理学药理学是指药理学的学科.

背景情况:

药物过度使用头痛 (MOH) 是慢性偏头痛的常见并发症.
众所周知,广泛用于缓解疼痛的非类固醇抗炎药物 (NSAIDs) 会破坏肠道屏障功能.
由于NSAID引起的漏肠和MOH病理生理学之间的联系尚不清楚.

研究的目的:

调查NSAID诱导的MOH与循环脂多糖结蛋白 (LBP) 水平的变化之间的关联.
检查炎症分子在MOH发展中的作用.
探索NSAID暴露对肠道屏障完整性和全身炎症的影响.

主要方法:

药物过度使用头痛 (MOH) 在雌性Sprague Dawley大鼠中被诱导,使用Piroxicam (10 mg/kg/day) 持续5周.
评估了疼痛行为,并收集血清和脑组织进行分析.
测量了LBP,紧结蛋白 (occludin,VE-cadherin) 和炎症标志物 (CGRP,IL-6,HMGB1,IL-17) 的水平.

主要成果:

皮罗西卡姆暴露显著增加了MOH的疼痛行为.
患有MOH的老鼠表现出LBP,CGRP,IL-6,IL-17,奥克卢丁和VE-cadherin的血清水平升高.
在皮罗西卡姆治疗组的大脑组织中观察到IL-17和HMGB1的水平增加.
血清LBP与肠道屏障标记物和炎症分子有正相关性,与疼痛值有负相关性.

结论:

在老鼠中,NSAID诱导的MOH与肠道屏障功能受损和全身LPS增加有关.
增加的LBP,VE-cadherin和ocludin水平表明肠道泄漏导致MOH.
诸如HMGB1,IL-6,IL-17和CGRP之类的炎症媒介可能在MOH病变发生过程中起着至关重要的作用.
准漏肠和促炎途径为MOH管理提供了潜在的治疗策略.

关键词:

这就是HMGB1的特点.它的IL-17是IL-17.炎症炎症是一种炎症.在 LBP LBP 中.在LPS中使用LPS.有漏洞的肠道 MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH MOH 偏头痛是一种偏头痛.欧克卢丁是一种隐蔽剂.这就是VECcadherin.

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