{"title":"Oleocanthal protects against neuronal inflammation and cardiopulmonary bypass surgery-induced brain injury in rats by regulating the NLRP3 pathway.","authors":"Xiuye Liu, Lijuan Yang, Li Wang, 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.
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.