Oleocanthal protects against neuronal inflammation and cardiopulmonary bypass surgery-induced brain injury in rats by regulating the NLRP3 pathway.

IF 1.9 4区 医学 Q4 NEUROSCIENCES
Xiuye Liu, Lijuan Yang, Li Wang, Qiongmei Guo
{"title":"Oleocanthal protects against neuronal inflammation and cardiopulmonary bypass surgery-induced brain injury in rats by regulating the NLRP3 pathway.","authors":"Xiuye Liu,&nbsp;Lijuan Yang,&nbsp;Li Wang,&nbsp;Qiongmei Guo","doi":"10.3233/RNN-201073","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Open heart surgery is performed with the aid of cardiopulmonary bypass (CPB) techniques that may cause neuronal injuries.</p><p><strong>Objective: </strong>This study investigated the potential protective effect of oleocanthal pre-treatment against CPB-induced cerebral injury.</p><p><strong>Methods: </strong>Oleocanthal 30 mg/kg i.p. was administered 3 h before CPB induction in the treated group. Behavioral neurological scores and cerebral injury were assessed to determine the effects of oleocanthal, based on oxidative stress and serum mediators of inflammation by enzyme-linked immunosorbent assay (ELISA). Quantitative Polymerase Chain Reaction (qRT-PCR) was used to estimate the mRNA expression of Toll-like receptor 4 (TLR4) and Interleukin 1 Receptor Associated Kinase 4 (IRAK4) proteins in the cerebral tissue of rats CPB-induced injury. Western blot assay and histopathology were also performed.</p><p><strong>Results: </strong>The findings suggest that pre-treatment with oleocanthal reduced neurological dysfunction and cerebral injury. Parameters of oxidative stress and cytokine levels were reduced in the serum of the oleocanthal treated group compared with the CPB-only group. Pre-treatment with oleocanthal ameliorated the expression of TLR-4, IRAK4, and Zonula occludens-1 (ZO-1) proteins in the cerebral tissue of the CPB-injured rats.</p><p><strong>Conclusions: </strong>The results revealed that treatment with oleocanthal protected against cerebral damage by controlling microglia inflammation through the TLR-4 pathway.</p>","PeriodicalId":21130,"journal":{"name":"Restorative neurology and neuroscience","volume":null,"pages":null},"PeriodicalIF":1.9000,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/RNN-201073","citationCount":"3","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Restorative neurology and neuroscience","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3233/RNN-201073","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 3

Abstract

Background: Open heart surgery is performed with the aid of cardiopulmonary bypass (CPB) techniques that may cause neuronal injuries.

Objective: This study investigated the potential protective effect of oleocanthal pre-treatment against CPB-induced cerebral injury.

Methods: Oleocanthal 30 mg/kg i.p. was administered 3 h before CPB induction in the treated group. Behavioral neurological scores and cerebral injury were assessed to determine the effects of oleocanthal, based on oxidative stress and serum mediators of inflammation by enzyme-linked immunosorbent assay (ELISA). Quantitative Polymerase Chain Reaction (qRT-PCR) was used to estimate the mRNA expression of Toll-like receptor 4 (TLR4) and Interleukin 1 Receptor Associated Kinase 4 (IRAK4) proteins in the cerebral tissue of rats CPB-induced injury. Western blot assay and histopathology were also performed.

Results: The findings suggest that pre-treatment with oleocanthal reduced neurological dysfunction and cerebral injury. Parameters of oxidative stress and cytokine levels were reduced in the serum of the oleocanthal treated group compared with the CPB-only group. Pre-treatment with oleocanthal ameliorated the expression of TLR-4, IRAK4, and Zonula occludens-1 (ZO-1) proteins in the cerebral tissue of the CPB-injured rats.

Conclusions: The results revealed that treatment with oleocanthal protected against cerebral damage by controlling microglia inflammation through the TLR-4 pathway.

油橄榄素通过调节NLRP3通路,对神经炎症和体外循环手术引起的大鼠脑损伤具有保护作用。
背景:心脏直视手术是在体外循环(CPB)技术的帮助下进行的,可能会导致神经元损伤。目的:探讨油橄榄素预处理对cpb所致脑损伤的潜在保护作用。方法:治疗组在CPB诱导前3 h给予油烛素30 mg/kg ig。通过酶联免疫吸附试验(ELISA)评估行为神经学评分和脑损伤,以确定油橄榄素的作用,基于氧化应激和血清炎症介质。采用定量聚合酶链反应(Quantitative Polymerase Chain Reaction, qRT-PCR)方法检测cpb损伤大鼠脑组织中toll样受体4 (TLR4)和白细胞介素1受体相关激酶4 (IRAK4)蛋白的mRNA表达。同时进行Western blot检测和组织病理学检查。结果:研究结果表明,油籽油预处理可减轻神经功能障碍和脑损伤。与单用cpb组相比,油酸果皮处理组血清中氧化应激参数和细胞因子水平降低。油棘醇预处理可改善cpb损伤大鼠脑组织中TLR-4、IRAK4和ZO-1蛋白的表达。结论:结果表明,油橄榄素治疗通过TLR-4通路控制小胶质细胞炎症,从而对脑损伤有保护作用。
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
CiteScore
5.40
自引率
3.60%
发文量
22
审稿时长
>12 weeks
期刊介绍: This interdisciplinary journal publishes papers relating to the plasticity and response of the nervous system to accidental or experimental injuries and their interventions, transplantation, neurodegenerative disorders and experimental strategies to improve regeneration or functional recovery and rehabilitation. Experimental and clinical research papers adopting fresh conceptual approaches are encouraged. The overriding criteria for publication are novelty, significant experimental or clinical relevance and interest to a multidisciplinary audience. Experiments on un-anesthetized animals should conform with the standards for the use of laboratory animals as established by the Institute of Laboratory Animal Resources, US National Academy of Sciences. Experiments in which paralytic agents are used must be justified. Patient identity should be concealed. All manuscripts are sent out for blind peer review to editorial board members or outside reviewers. Restorative Neurology and Neuroscience is a member of Neuroscience Peer Review Consortium.
×
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