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Nicole Arend, Susanna Koenig, Peter Laubichler, Armin Wolf, Christos Haritoglou, Michael W. Ulbig, Anselm Kampik, Marcus Kernt; Idebenone Prevents Retinal Pigmentepithelium (RPE) Cells from Oxidative Stress and Senescence. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6887.
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© ARVO (1962-2015); The Authors (2016-present)
Age related macular degeneration (AMD) is one of the leading causes of blindness. Oxidative stress plays an important role in the pathogenesis of this disease. This study investigates the potential anti-apoptotic and cytoprotective effects of idebenone on retinal pigment epithelial cells (ARPE19) under oxidative stress.
ARPE19 were treated with 1 to 100 µM idebenone. Cell viability (MTT assay and live-dead assay), induction of intracellular reactive oxygen species (ROS) and senescence-associated β-galactosidase (SA β-Gal) activity were investigated. In addition, expression of BAX and Bcl-2, and their mRNA were determined after 48 h and after H2O2 treatment.
Idebenone concentrations from 1 to 20 µM showed no toxic effects on ARPE19. Pretreatment with 5 and 7.5 µM idebenone led to an increase in viability of ARPE19 after H2O2 treatment. In addition, idebenone pretreatment significantly attenuated the induction of SA β-Gal and intracellular ROS after treatment with H2O2. When ARPE19 were treated with idebenone and H2O2, rt-PCR and Western blot analysis yielded a trend towards, but no significant increase in expression of Bcl-2 and decrease of BAX, compared to those cells that were treated with H2O2 only.
In this study idebenone increased survival of ARPE19 cells and reduced senescence and oxidative stress. Our results suggest that idebenone may help to protect the RPE against oxidative stress. However, these effects may be modulated by of other pathways than the Bcl-2/BAX pathway.
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