Nicotinamide adenine dinucleotide alleviates neuroinflammation in rats with traumatic brain injury

IF 2.5 4区医学 Q3 NEUROSCIENCES Neuroscience Letters Pub Date : 2025-02-22 DOI:10.1016/j.neulet.2025.138178

Huancheng Wu , Mengli Jin , Jiandong Hu , Fenge Li

{"title":"Nicotinamide adenine dinucleotide alleviates neuroinflammation in rats with traumatic brain injury","authors":"Huancheng Wu , Mengli Jin , Jiandong Hu , Fenge Li","doi":"10.1016/j.neulet.2025.138178","DOIUrl":null,"url":null,"abstract":"<div><h3>Objective</h3><div>To characterize the pathology and pathophysiological processes within 6 h after Traumatic brain injury (TBI) in rats, elucidate the neuroprotective effects and the underlying mechanisms of Nicotinamide Adenine Dinucleotide (NAD) in the early stage of TBI to explore the feasibility and clinical benefits of applying NAD directly to the localized injury after TBI.</div></div><div><h3>Material and Methods</h3><div>54 male Sprague-Dawley (SD) rats aged 6–8 weeks were randomly assigned equally to three groups, sham-operated surgery (SO) with saline treatment (SO + Saline), TBI with saline treatment (TBI + Saline), and TBI with 10 μM NAD treatment (TBI + NAD). The whole brain tissues were collected at 1, 3, and 6 h following the procedure. Levels of biomarkers for TBI including S100β, TNF-α, occludin, PPARβ/δ were measured.</div></div><div><h3>Results</h3><div>Significant neuroinflammation was observed in the rat brains after TBI, which peaked at 3 h following injury. Significant changes in S100β, TNF-α, PPARβ/δ, and occluding were also observed. Treatment with NAD significantly alleviated neuroinflammation at 1 h following TBI.</div></div><div><h3>Conclusions</h3><div>TBI caused severe neuroinflammation in rat brains, which peaked at 3 h following injury. Treatment with NAD alleviated neuroinflammation in TBI rats.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"852 ","pages":"Article 138178"},"PeriodicalIF":2.5000,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroscience Letters","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0304394025000667","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}

引用次数: 0

Abstract

Objective

To characterize the pathology and pathophysiological processes within 6 h after Traumatic brain injury (TBI) in rats, elucidate the neuroprotective effects and the underlying mechanisms of Nicotinamide Adenine Dinucleotide (NAD) in the early stage of TBI to explore the feasibility and clinical benefits of applying NAD directly to the localized injury after TBI.

Material and Methods

54 male Sprague-Dawley (SD) rats aged 6–8 weeks were randomly assigned equally to three groups, sham-operated surgery (SO) with saline treatment (SO + Saline), TBI with saline treatment (TBI + Saline), and TBI with 10 μM NAD treatment (TBI + NAD). The whole brain tissues were collected at 1, 3, and 6 h following the procedure. Levels of biomarkers for TBI including S100β, TNF-α, occludin, PPARβ/δ were measured.

Results

Significant neuroinflammation was observed in the rat brains after TBI, which peaked at 3 h following injury. Significant changes in S100β, TNF-α, PPARβ/δ, and occluding were also observed. Treatment with NAD significantly alleviated neuroinflammation at 1 h following TBI.

Conclusions

TBI caused severe neuroinflammation in rat brains, which peaked at 3 h following injury. Treatment with NAD alleviated neuroinflammation in TBI rats.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

求助全文

约1分钟内获得全文去求助

来源期刊

Neuroscience Letters 医学-神经科学

CiteScore

5.20

自引率

0.00%

发文量

408

审稿时长

50 days

期刊介绍： Neuroscience Letters is devoted to the rapid publication of short, high-quality papers of interest to the broad community of neuroscientists. Only papers which will make a significant addition to the literature in the field will be published. Papers in all areas of neuroscience - molecular, cellular, developmental, systems, behavioral and cognitive, as well as computational - will be considered for publication. Submission of laboratory investigations that shed light on disease mechanisms is encouraged. Special Issues, edited by Guest Editors to cover new and rapidly-moving areas, will include invited mini-reviews. Occasional mini-reviews in especially timely areas will be considered for publication, without invitation, outside of Special Issues; these un-solicited mini-reviews can be submitted without invitation but must be of very high quality. Clinical studies will also be published if they provide new information about organization or actions of the nervous system, or provide new insights into the neurobiology of disease. NSL does not publish case reports.