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논문 기본 정보

자료유형
학술저널
저자정보
박지영 (제주대학교) Xia Han (제주대학교) 박미경 (제주대학교) 오민창 (제주대학교) Pattage Madushan Dilhara Jayatissa Fernando (제주대학교) 강경아 (제주대학교) 류예성 (제주대학교) 정우희 (한국원자력연구원) 김인규 (한국원자력연구원) 현진원 (제주대학교)
저널정보
대한암예방학회 대한암예방학회지 대한암예방학회지 제21권 제1호
발행연도
2016.1
수록면
41 - 47 (7page)

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Background: Hyperoside, a flavonoid which is mainly found in Hypericum perforatum L., has many biological effects. One of the most important effects is to prevent the oxidative stress induced by reactive oxygen species. However, the molecular mechanisms underlying its effect are not fully understood. Oxidative stress is implicated in the occurrence of various physical diseases. A wide array of enzymatic antioxidant defense systems include NADH: quinone oxidoreductase 1, superoxide dismutase, and heme oxygenase-1 (HO-1). In the present study, the protective effects of hyperoside against hydrogen peroxide-induced oxidative stress in human lens epithelial cells, HLE-B3, were investigated in terms of HO-1 induction. Methods: The protein and mRNA expressions of HO-1 were examined by Western blotting and reverse transcriptase-PCR assays, respectively. To evaluate the ability of hyperoside to activate nuclear factor erythroid 2-related factor 2 (Nrf2), Western blotting and electrophoretic mobility shift assay were performed with nuclear extracts prepared from HLE-B3 cells treated with hyperoside. The activation of extracellular signal-regulated kinase (ERK), the upstream kinase of Nrf2 signaling, was monitored by Western blot analysis. The protective effect of hyperoside in HLE-B3 cells against hydrogen peroxide was performed by MTT assay. Results: Hyperoside increased both the mRNA and protein expression of HO-1 in a time- and dose-dependent manner. In addition, hyperoside elevated the level of of Nrf2 and its antioxidant response element-binding activity, which was modulated by upstream of ERK. Moreover, it activated ERK and restored cell viability which was decreased by hydrogen peroxide. Conclusions: Hyperoside is an effective compound to protect cells against oxidative stress via HO-1 induction.

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