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학술저널
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한국미생물생명공학회 Journal of Microbiology and Biotechnology Journal of Microbiology and Biotechnology 제24권 제5호
발행연도
2014.1
수록면
605 - 613 (9page)

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We have previously shown that paraquat (PQ)-induced oxidative stress causes dramaticdamage in various human cell lines. Naringenin (NG) is an active flavanone, which has beenreported to have beneficial bioactivities, including antioxidative, anti-inflammatory, andantitumorigenic activities, with a relatively low toxicity to normal cells. In this study, weintended to assess the cytoprotective effect of NG against PQ-induced toxicity in the humanbronchial epithelial BEAS-2B cell line. Co-treatment with NG in PQ-treated BEAS-2B cells canreduce PQ-induced cellular toxicity. NG can also decrease the generation of intracellular ROScaused by PQ treatment. We also observed that treatment with NG in PQ-exposed BEAS-2Bcells 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 andpromote its nuclear translocation. In addition, NG co-treatment can induce the expression ofNRF2-downstream target genes such as that of heme oxygenase-1 (HO-1) and NAD(P)H:quinoneoxidoreductase 1 (NQO1). A small interfering RNA study revealed that the knockdown ofNRF2 can abrogate NG-mediated protection of the cells from PQ-induced cellular toxicity. Wepropose that NG effectively alleviates PQ-induced cytotoxicity in human bronchial epithelialBEAS-2B cells through the NRF2-regulated antioxidant defense pathway, and NG might be agood therapeutic candidate molecule in oxidative stress-related diseases.

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