Cytoprotective effect of rhamnetin on miconazole-induced H9c2 cell damage

저작시기 2015.12 |등록일 2016.02.11 파일확장자어도비 PDF (pdf) | 6페이지 | 가격 6,000원
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발행기관 : 대한지역사회영양학회 수록지정보 : Nutrition Research and Practice / 9권 / 6호
저자명 : Kang Pa Lee, Jai-Eun Kim, Won-Hwan Park



영어 초록

BACKGROUND/OBJECTIVES: Reactive oxygen species (ROS) formation is closely related to miconazole-induced heart dysfunction. Although rhamnetin has antioxidant effects, it remained unknown whether it can protect against miconazole-induced cardiomyocyte apoptosis. Thus, we investigated the effects of rhamnetin on miconazole-stimulated H9c2 cell apoptosis.
MATERIALS/METHODS: Cell morphology was observed by inverted microscope and cell viability was determined using a WelCount™ cell proliferation assay kit. Miconazole-induced ROS production was evaluated by fluorescence-activated cell sorting with 6-carboxy-2 ʹ,7ʹ-dichlorofluoroscein diacetate (H₂DCF-DA) stain. Immunoblot analysis was used to determine apurinic/apyrimidinic endonuclease 1 (APE/Ref-1) and cleaved cysteine-aspartic protease (caspase) 3 expression. NADPH oxidase levels were measured using real-time polymerase chain reaction.
RESULTS: Miconazole (3 and 10 μM) induced abnormal morphological changes and cell death in H9c2 cells. Rhamnetin enhanced the viability of miconazole (3 μM)-treated cells in a dose-dependent manner. Rhamnetin (1 and 3 μM) treatment downregulated cleaved caspase 3 and upregulated APE/Ref-1 expression in miconazole-stimulated cells. Additionally, rhamnetin significantly reduced ROS generation.
CONCLUSIONS: Our data suggest that rhamnetin may have cytoprotective effects in miconazole-stimulated H9c2 cardiomyocytes via ROS inhibition. This effect most likely occurs through the upregulation of APE/Ref-1 and attenuation of hydrogen peroxide levels.

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