December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Prevention of oxidative stress induced RPE death by PPAR agonists
Author Affiliations & Notes
  • JY Chang
    Anatomy & Neurobiology Ophthalmology
    Univ Arkansas for Medical Sciences Little Rock AR
  • TK Garg
    Anatomy & Neurobiology
    Univ Arkansas for Medical Sciences Little Rock AR
  • Footnotes
    Commercial Relationships   J.Y. Chang, None; T.K. Garg, None.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 673. doi:
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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)

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Abstract

Abstract: : 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.

Keywords: 308 age-related macular degeneration • 504 oxidation/oxidative or free radical damage • 567 retinal pigment epithelium 
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