Naringenin Exerts Cytoprotective Effect Against Paraquat-Induced Toxicity in Human Bronchial Epithelial BEAS-2B Cells Through NRF2 Activation
- Authors
- Podder, Biswajit; Song, Ho-Yeon; Kim, Yong-Sik
- Issue Date
- May-2014
- Publisher
- 한국미생물·생명공학회
- Keywords
- Naringenin; paraquat; antioxidant-related genes; human bronchial epithelial BEAS-2B cells
- Citation
- Journal of Microbiology and Biotechnology, v.24, no.5, pp 605 - 613
- Pages
- 9
- Journal Title
- Journal of Microbiology and Biotechnology
- Volume
- 24
- Number
- 5
- Start Page
- 605
- End Page
- 613
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/12225
- DOI
- 10.4014/jmb.1402.02001
- ISSN
- 1017-7825
1738-8872
- 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.
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Collections - College of Medicine > Department of Microbiology > 1. Journal Articles
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