Naringenin Exerts Cytoprotective Effect Against Paraquat-Induced Toxicity in Human Bronchial Epithelial BEAS-2B Cells Through NRF2 Activation
DC Field | Value | Language |
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dc.contributor.author | Podder, Biswajit | - |
dc.contributor.author | Song, Ho-Yeon | - |
dc.contributor.author | Kim, Yong-Sik | - |
dc.date.accessioned | 2021-08-11T22:46:28Z | - |
dc.date.available | 2021-08-11T22:46:28Z | - |
dc.date.issued | 2014-05 | - |
dc.identifier.issn | 1017-7825 | - |
dc.identifier.issn | 1738-8872 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/12225 | - |
dc.description.abstract | We have previously shown that paraquat (PQ)-induced oxidative stress causes dramatic damage in various human cell lines. Naringenin (NG) is an active flavanone, which has been reported to have beneficial bioactivities, including antioxidative, anti-inflammatory, and antitumorigenic activities, with a relatively low toxicity to normal cells. In this study, we intended to assess the cytoprotective effect of NG against PQ-induced toxicity in the human bronchial epithelial BEAS-2B cell line. Co-treatment with NG in PQ-treated BEAS-2B cells can reduce PQ-induced cellular toxicity. NG can also decrease the generation of intracellular ROS caused by PQ treatment. We also observed that treatment with NG in PQ-exposed BEAS-2B cells can significantly induce the expression of antioxidant-related genes, including GPX2, GPX3, GPX5, and GPX7. NG co-treatment can also activate the NRF2 transcription factor and promote its nuclear translocation. In addition, NG co-treatment can induce the expression of NRF2-downstream target genes such as that of heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1). A small interfering RNA study revealed that the knockdown of NRF2 can abrogate NG-mediated protection of the cells from PQ-induced cellular toxicity. We propose that NG effectively alleviates PQ-induced cytotoxicity in human bronchial epithelial BEAS-2B cells through the NRF2-regulated antioxidant defense pathway, and NG might be a good therapeutic candidate molecule in oxidative stress-related diseases. | - |
dc.format.extent | 9 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | 한국미생물·생명공학회 | - |
dc.title | Naringenin Exerts Cytoprotective Effect Against Paraquat-Induced Toxicity in Human Bronchial Epithelial BEAS-2B Cells Through NRF2 Activation | - |
dc.type | Article | - |
dc.publisher.location | 대한민국 | - |
dc.identifier.doi | 10.4014/jmb.1402.02001 | - |
dc.identifier.scopusid | 2-s2.0-84901014569 | - |
dc.identifier.wosid | 000336511400004 | - |
dc.identifier.bibliographicCitation | Journal of Microbiology and Biotechnology, v.24, no.5, pp 605 - 613 | - |
dc.citation.title | Journal of Microbiology and Biotechnology | - |
dc.citation.volume | 24 | - |
dc.citation.number | 5 | - |
dc.citation.startPage | 605 | - |
dc.citation.endPage | 613 | - |
dc.type.docType | Article | - |
dc.identifier.kciid | ART001877654 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
dc.relation.journalResearchArea | Biotechnology & Applied Microbiology | - |
dc.relation.journalResearchArea | Microbiology | - |
dc.relation.journalWebOfScienceCategory | Biotechnology & Applied Microbiology | - |
dc.relation.journalWebOfScienceCategory | Microbiology | - |
dc.subject.keywordPlus | TRANSCRIPTION FACTOR NRF2 | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | MICE | - |
dc.subject.keywordPlus | ANTIOXIDANTS | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | FLAVONOIDS | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | TARGET | - |
dc.subject.keywordPlus | GENES | - |
dc.subject.keywordAuthor | Naringenin | - |
dc.subject.keywordAuthor | paraquat | - |
dc.subject.keywordAuthor | antioxidant-related genes | - |
dc.subject.keywordAuthor | human bronchial epithelial BEAS-2B cells | - |
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