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JY Chang, TK Garg; Prevention of oxidative stress induced RPE death by PPAR agonists . Invest. Ophthalmol. Vis. Sci. 2002;43(13):673.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Cellular response to and potential pharmacological intervention for oxidative stress in human RPE were investigated. Method: Primary cultures of human RPE and the RPE cell line, ARPE-19, were treated with H2O2, and the effects of oxidative stress were analyzed by the MTT viability assay, immunohistochemistry and Western blot analyses. Results: The degree of oxidative stress induced cytotoxicity is determined by the concentration of H2O2, the duration of treatment and the density of RPE used in the experiments. Oxidative stress caused an up-regulation of the ERK MAP kinase activity within an hour as determined by the immunohistochemical staining and the Western blot analysis. Pretreatment of cells with the PPARgamma agonist, 15d-PGJ2 greatly attenuated the oxidative stress induced cytotoxicity. Conclusion: MAP kinase activation is an early event associated with oxidative stress in human RPE. Agonists for PPARgamma can be used as a pharmacological intervention for oxidative stress induced cytotoxicity.
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