Antinociceptive effect of N-acetyl glucosamine in a rat model of neuropathic pain.

IF 3.8 4区 医学 Q1 Medicine
Acta Neuropsychiatrica Pub Date : 2022-10-01 Epub Date: 2022-02-03 DOI:10.1017/neu.2022.3
Ehsan Mohebbi, Mehdi Molavi, Mohamadreza Amin, Bahareh Amin, Mohammad Sahebkar
{"title":"Antinociceptive effect of N-acetyl glucosamine in a rat model of neuropathic pain.","authors":"Ehsan Mohebbi,&nbsp;Mehdi Molavi,&nbsp;Mohamadreza Amin,&nbsp;Bahareh Amin,&nbsp;Mohammad Sahebkar","doi":"10.1017/neu.2022.3","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study was aimed at evaluating the efficacy of glucosamine and potential mechanisms of actions in a neuropathic pain model in rats.</p><p><strong>Methods: </strong>Glucosamine (500, 1000 and 2000 mg/kg) was administered via gavage route, 1 day before the chronic constriction injury (CCI) of sciatic nerve and daily for 14 days (prophylactic regimen), or from days 5 to 14 post-injury (therapeutic regimen), as the indicators of neuropathic pain, mechanical allodynia, cold allodynia and thermal hyperalgesia were assessed on days 0, 3, 5, 7, 10 and 14 after ligation. Inducible nitric oxide synthase (iNOS) and tumour necrosis factor alpha (TNF-α) gene expressions were measured by real-time polymerase chain reaction. TNF-α protein content was measured using the enzyme-linked immunosorbent assay method.</p><p><strong>Results: </strong>Three days after nerve injury, the threshold of pain was declined among animals subjected to neuropathic pain. Mechanical and cold allodynia, as well as thermal hyperalgesia were attenuated by glucosamine (500, 1000, 2000 mg/kg) in the prophylactic regimen. However, existing pain was not decreased by this drug. Increased mRNA expression of iNOS and TNF-α was significantly reduced in the spinal cord of CCI animals by glucosamine (500, 1000, 2000 mg/kg) in the prophylactic regimen. The overall expression of spinal TNF-α was increased by CCI, but this increase was reduced in animals receiving glucosamine prophylactic treatment.</p><p><strong>Conclusion: </strong>Findings suggest that glucosamine as a safe supplement may be a useful candidate in preventing neuropathic pain following nerve injury. Antioxidant and anti-inflammatory effects may be at least in part responsible for the antinociceptive effects of this drug.</p>","PeriodicalId":7066,"journal":{"name":"Acta Neuropsychiatrica","volume":null,"pages":null},"PeriodicalIF":3.8000,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta Neuropsychiatrica","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1017/neu.2022.3","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/2/3 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0

Abstract

Objective: This study was aimed at evaluating the efficacy of glucosamine and potential mechanisms of actions in a neuropathic pain model in rats.

Methods: Glucosamine (500, 1000 and 2000 mg/kg) was administered via gavage route, 1 day before the chronic constriction injury (CCI) of sciatic nerve and daily for 14 days (prophylactic regimen), or from days 5 to 14 post-injury (therapeutic regimen), as the indicators of neuropathic pain, mechanical allodynia, cold allodynia and thermal hyperalgesia were assessed on days 0, 3, 5, 7, 10 and 14 after ligation. Inducible nitric oxide synthase (iNOS) and tumour necrosis factor alpha (TNF-α) gene expressions were measured by real-time polymerase chain reaction. TNF-α protein content was measured using the enzyme-linked immunosorbent assay method.

Results: Three days after nerve injury, the threshold of pain was declined among animals subjected to neuropathic pain. Mechanical and cold allodynia, as well as thermal hyperalgesia were attenuated by glucosamine (500, 1000, 2000 mg/kg) in the prophylactic regimen. However, existing pain was not decreased by this drug. Increased mRNA expression of iNOS and TNF-α was significantly reduced in the spinal cord of CCI animals by glucosamine (500, 1000, 2000 mg/kg) in the prophylactic regimen. The overall expression of spinal TNF-α was increased by CCI, but this increase was reduced in animals receiving glucosamine prophylactic treatment.

Conclusion: Findings suggest that glucosamine as a safe supplement may be a useful candidate in preventing neuropathic pain following nerve injury. Antioxidant and anti-inflammatory effects may be at least in part responsible for the antinociceptive effects of this drug.

n -乙酰氨基葡萄糖在神经性疼痛大鼠模型中的抗伤害性作用。
目的:探讨氨基葡萄糖对大鼠神经性疼痛模型的影响及其作用机制。方法:在坐骨神经慢性收缩损伤(CCI)前1天、预防组或损伤后第5 ~ 14天(治疗组)每日灌胃给药葡萄糖胺500、1000、2000 mg/kg,分别于结扎后第0、3、5、7、10、14天评估神经性疼痛、机械异位性疼痛、冷异位性疼痛和热痛觉过敏指标。实时聚合酶链反应检测诱导型一氧化氮合酶(iNOS)和肿瘤坏死因子α (TNF-α)基因表达。采用酶联免疫吸附法测定TNF-α蛋白含量。结果:神经损伤后3 d,神经性疼痛动物的痛觉阈值下降。在预防方案中,葡萄糖胺(500、1000、2000 mg/kg)可减轻机械性和冷性异常痛以及热痛觉过敏。然而,这种药物并没有减轻现有的疼痛。葡萄糖胺(500、1000、2000 mg/kg)预防组显著降低CCI动物脊髓iNOS和TNF-α mRNA表达的升高。脊髓TNF-α的总体表达在CCI中升高,但在接受氨基葡萄糖预防治疗的动物中,这种升高有所降低。结论:研究结果表明,氨基葡萄糖作为一种安全的补充物可能是预防神经损伤后神经性疼痛的有效候选药物。抗氧化和抗炎作用可能至少是这种药物的抗伤害作用的部分原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Acta Neuropsychiatrica
Acta Neuropsychiatrica 医学-精神病学
CiteScore
8.50
自引率
5.30%
发文量
30
审稿时长
6-12 weeks
期刊介绍: Acta Neuropsychiatrica is an international journal focussing on translational neuropsychiatry. It publishes high-quality original research papers and reviews. The Journal''s scope specifically highlights the pathway from discovery to clinical applications, healthcare and global health that can be viewed broadly as the spectrum of work that marks the pathway from discovery to global health.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信