Naringenin Exhibits Antiglioma Activity Related to Aryl Hydrocarbon Receptor Activity and IL-6, CCL2, and TNF-α Expression.

IF 2.7 3区医学 Q3 NEUROSCIENCES

Brain Sciences Pub Date : 2025-03-20 DOI:10.3390/brainsci15030325

Monique Reis de Santana, Deivison Silva Argolo, Irlã Santos Lima, Cleonice Creusa Dos Santos, Maurício Moraes Victor, Gabriel Dos Santos Ramos, Ravena Pereira do Nascimento, Henning Ulrich, Silvia Lima Costa

{"title":"Naringenin Exhibits Antiglioma Activity Related to Aryl Hydrocarbon Receptor Activity and IL-6, CCL2, and TNF-α Expression.","authors":"Monique Reis de Santana, Deivison Silva Argolo, Irlã Santos Lima, Cleonice Creusa Dos Santos, Maurício Moraes Victor, Gabriel Dos Santos Ramos, Ravena Pereira do Nascimento, Henning Ulrich, Silvia Lima Costa","doi":"10.3390/brainsci15030325","DOIUrl":null,"url":null,"abstract":"Background: Glioblastoma (GBM) is a highly aggressive brain tumor characterized by rapid cell proliferation, invasive behavior, and chemoresistance. The aryl hydrocarbon receptor (AhR) is implicated in chemoresistance and immune evasion, making it a promising therapeutic target. Natural compounds such as flavonoids have gained attention for their anti-inflammatory, antioxidant, and anticancer properties. Among them, naringenin, a citrus-derived flavonoid, exerts antiproliferative, pro-apoptotic, and immunomodulatory effects.Objectives: This study investigated the antiglioma effects of the flavonoid naringenin on the viability, growth, and migration of glioma cells and its potential role as an AhR modulator.Methods: Human (U87) and rat (C6) glioma cell lines were exposed to naringenin (10-300 µM) alone or in combination with the AhR agonist indole-3-carbinol (50 µM) for 24 to 48 h. Cell viability, scratch wound, and cell migration assays were performed. The expression of inflammatory markers was also analyzed by RT-qPCR.Results: Naringenin exerted dose- and time-dependent inhibition of cell viability and migration. The treatment decreased the gene expression of interleukin-6 (IL-6) and chemokine (CCL2), alongside increased tumor necrosis factor-alpha (TNF-α) expression, an effect reversed by the AhR agonist.Conclusions: These findings highlight naringenin's potential as an antiglioma agent and its role in AhR signaling.","PeriodicalId":9095,"journal":{"name":"Brain Sciences","volume":"15 3","pages":""},"PeriodicalIF":2.7000,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11940588/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain Sciences","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3390/brainsci15030325","RegionNum":3,"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

Background: Glioblastoma (GBM) is a highly aggressive brain tumor characterized by rapid cell proliferation, invasive behavior, and chemoresistance. The aryl hydrocarbon receptor (AhR) is implicated in chemoresistance and immune evasion, making it a promising therapeutic target. Natural compounds such as flavonoids have gained attention for their anti-inflammatory, antioxidant, and anticancer properties. Among them, naringenin, a citrus-derived flavonoid, exerts antiproliferative, pro-apoptotic, and immunomodulatory effects.

Objectives: This study investigated the antiglioma effects of the flavonoid naringenin on the viability, growth, and migration of glioma cells and its potential role as an AhR modulator.

Methods: Human (U87) and rat (C6) glioma cell lines were exposed to naringenin (10-300 µM) alone or in combination with the AhR agonist indole-3-carbinol (50 µM) for 24 to 48 h. Cell viability, scratch wound, and cell migration assays were performed. The expression of inflammatory markers was also analyzed by RT-qPCR.

Results: Naringenin exerted dose- and time-dependent inhibition of cell viability and migration. The treatment decreased the gene expression of interleukin-6 (IL-6) and chemokine (CCL2), alongside increased tumor necrosis factor-alpha (TNF-α) expression, an effect reversed by the AhR agonist.

Conclusions: These findings highlight naringenin's potential as an antiglioma agent and its role in AhR signaling.

查看原文本刊更多论文

求助全文

约1分钟内获得全文求助全文

来源期刊

Brain Sciences Neuroscience-General Neuroscience

CiteScore

4.80

自引率

9.10%

发文量

1472

审稿时长

18.71 days

期刊介绍： Brain Sciences (ISSN 2076-3425) is a peer-reviewed scientific journal that publishes original articles, critical reviews, research notes and short communications in the areas of cognitive neuroscience, developmental neuroscience, molecular and cellular neuroscience, neural engineering, neuroimaging, neurolinguistics, neuropathy, systems neuroscience, and theoretical and computational neuroscience. Our aim is to encourage scientists to publish their experimental and theoretical results in as much detail as possible. There is no restriction on the length of the papers. The full experimental details must be provided so that the results can be reproduced. Electronic files or software regarding the full details of the calculation and experimental procedure, if unable to be published in a normal way, can be deposited as supplementary material.