快速眼动睡眠剥夺雄性Wistar大鼠给予抗tnf -α后疼痛耐受阈值的评价

M. Hosseinpourfard, M. Nasehi, M. Zarrindast, M. Izadi, M. Nami
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引用次数: 0

摘要

背景与目的:快速眼动(REM)睡眠剥夺后肿瘤坏死因子α (TNF-α)水平的变化。TNF-α是REM睡眠剥夺(RSD)的已知生物标志物。先前的研究表明,快速眼动睡眠的任何改变都会增加TNF-α的含量。因此,在使用抗tnf -α或英夫利昔单抗(IFX)后,失眠患者的疼痛耐受阈值(PTT)被认为增加。本研究旨在证明IFX在医院住院病人疼痛管理中的作用及其重要性。方法与材料/患者:经德黑兰医科大学伦理委员会批准,分为9组,雄性Wistar大鼠72只。协议-女性- 940816)。用Remicade诱导抗tnf -α。采用多平台水箱进行快速眼动睡眠剥夺诱导。在热板仪上测量疼痛耐受性。结果:生理盐水组大鼠对热板的耐受时间较IFX (0.2 mg/kg)组明显增加(F2=8.363) (P<0.001)。结论:慢性SD可引起神经炎性损伤。从长远来看,快速眼动睡眠剥夺会通过炎症机制,在一定程度上通过tnf α相关途径,使大脑对神经退行性损伤变得敏感。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Evaluation of Pain Tolerance Threshold Following Administration of Anti-TNF-α in REM Sleep-deprived Male Wistar Rats
Background and Aim: The level of Tumor Necrosis Factor-alpha (TNF-α) changes by Rapid Eye Movement (REM) sleep deprivation. TNF-α is a known biomarker of REM Sleep Deprivation (RSD). Prior studies have shown that any alteration in REM sleep can increase the amount of TNF-α. Accordingly, the Pain Tolerance Threshold (PTT) is believed to be increased in patients with insomnia after using anti-TNF-α or Infliximab (IFX). The present study aims to demonstrate the effect of IFX and its importance in the pain management of hospital inpatients. Methods and Materials/Patients: Seventy-two male Wistar rats in 9 groups were studied after obtaining the approval of the ethics committee of Tehran University of Medical Sciences (CNS. Protocol-ICSS-940816). Remicade was used for inducing the anti-TNF-α. Multiple platform water-tank was used for REM sleep deprivation induction. Pain tolerance was measured on a hot plate apparatus. Results: There was a significant increase in the duration of the rats’ tolerance on the hot plate between the saline group and the group that received IFX (0.2 mg/kg) (F2=8.363) (P<0.001). Conclusion: Chronic SD can cause neuronal damage due to neuroinflammatory insults. REM sleep deprivation, in the long run, sensitizes the brain to neurodegenerative insults via the inflammatory mechanism, to some extent through the TNFα-associated pathways.
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