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논문 기본 정보

자료유형
학술저널
저자정보
Rui Zhang (Jeju National University School of Medicine and Jiangsu University China) 박미경 (제주대학교) Min Chang Oh (Department of Biochemistry Jeju National University School of Medicine Jeju) Jeong Eon Park (Department of Biochemistry Jeju National University School of Medicine) Kristina Shilnikova (Department of Biochemistry Jeju National University School of Medicine Jeju Korea) Yu Jin Moon (Department of Biochemistry Jeju National University School of Medicine Jeju Korea) Dong Hyun Kim (College of Pharmacy Kyung Hee University) 정우희 (한국원자력연구원) In Gyu Kim (Koea Atomic Energy Research Institute) 현진원 (제주대학교)
저널정보
대한암예방학회 대한암예방학회지 대한암예방학회지 제21권 제4호
발행연도
2016.1
수록면
257 - 263 (7page)

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Background: Isoflavones are biologically active compounds that occur naturally in a variety of plants, with relatively high levels in soybean. Tectorigenin, an isoflavone, protects against hydrogen peroxide (H2O2)-induced cell damage. However, the underlying mechanism is unknown. Methods: The MTT assay was performed to determine cell viability. Catalase activity was assessed by determining the amount of enzyme required to degrade 1 μM H2O2. Protein expression of catalase, phospho-extracellular signal-regulated kinase (ERK), IκB-α, and NF-κB were evaluated by Western blot analysis. A mobility shift assay was performed to assess the DNA-binding ability of NF-κB. Transient transfection and a NF-κB luciferase assay were performed to assess transcriptional activity. Results: Tectorigenin reduced H2O2-induced death of Chinese hamster lung fibroblasts (V79-4). In addition, tectorigenin increased the activity and protein expression of catalase. Blockade of catalase activity attenuated the protective effect of tectorigenin against oxidative stress. Furthermore, tectorigenin enhanced phosphorylation of ERK and nuclear expression of NF-B, while inhibition of ERK and NF-κB attenuated the protective effect of tectorigenin against oxidative stress. Conclusions: Tectorigenin protects cells against oxidative damage by activating catalase and modulating the ERK and NF-κB signaling pathway.

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