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Retino-protective effect of Bucida buceras against oxidative stress induced by H(2)O(2) in human retinal pigment epithelial cells line
BACKGROUND: Reactive Oxygen Species (ROS) impair the physiological functions of Retinal Pigment Epithelial (RPE) cells, which are known as one major cause of age-related macular degeneration and retinopathy diseases. The purpose of this study is to explore the cytoprotective effects of the antioxida...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4518513/ https://www.ncbi.nlm.nih.gov/pubmed/26219933 http://dx.doi.org/10.1186/s12906-015-0765-6 |
Sumario: | BACKGROUND: Reactive Oxygen Species (ROS) impair the physiological functions of Retinal Pigment Epithelial (RPE) cells, which are known as one major cause of age-related macular degeneration and retinopathy diseases. The purpose of this study is to explore the cytoprotective effects of the antioxidant Bucida buceras extract in co-treatment with hydrogen peroxide (H(2)O(2)) delivery as a single addition or with continuous generation using glucose oxidase (GOx) in ARPE-19 cell cultures. The mechanism of Bucida buceras extract is believed to be associated with their antioxidant capacity to protect cells against oxidative stress. METHODS: A comparative oxidative stress H(2)O(2)-induced was performed by addition and enzymatic generation using glucose oxidase on human retinal pigment epithelial cells line. H(2)O(2)-induced injury was measured by toxic effects (cell death and apoptotic pathway) and intracellular redox status: glutathione (GSH), antioxidant enzymes (catalase and glutathione peroxidase) and reducing power (FRAP). The retino-protective effect of co-treatment with Bucida buceras extract on H(2)O(2)-induced human RPE cell injury was investigated by cell death (MTT assay) and oxidative stress biomarkers (H(2)O(2,) GSH, CAT, GPx and FRAP). RESULTS: Bucida buceras L. extract is believed to be associated with the ability to prevent cellular oxidative stress. When added as a pulse, H(2)O(2) is rapidly depleted and the cytotoxicity analyses show that cells can tolerate short exposure to high peroxide doses delivered as a pulse but are susceptible to lower chronic doses. Co-treatment with Bucida buceras was able to protect the cells against H(2)O(2)-induced injury. In addition to preventing cell death treatment with antioxidant plant could also reverse the significant decrease in GSH level, catalase activity and reducing power caused by H(2)O(2). CONCLUSION: These findings suggest that Bucida buceras could protect RPE against ocular pathogenesis associated with oxidative stress induced by H(2)O(2)-delivered by addition and enzymatic generation. |
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