June 2015
Volume 56, Issue 7
ARVO Annual Meeting Abstract  |   June 2015
Sulforaphane Inhibits Retinal Cell Death in Ischemia/Hypoxia
Author Affiliations & Notes
  • Lindsay Ambrecht
    Ophthalmology, Loyola Univ Med Center, Maywood, IL
  • Zhai Yougan
    Ophthalmology, Loyola Univ Med Center, Maywood, IL
  • James F McDonnell
    Ophthalmology, Loyola Univ Med Center, Maywood, IL
  • Jay Ira Perlman
    Ophthalmology, Loyola Univ Med Center, Maywood, IL
  • Footnotes
    Commercial Relationships Lindsay Ambrecht, None; Zhai Yougan, None; James McDonnell, None; Jay Perlman, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 32. doi:
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      Lindsay Ambrecht, Zhai Yougan, James F McDonnell, Jay Ira Perlman; Sulforaphane Inhibits Retinal Cell Death in Ischemia/Hypoxia. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):32.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: Retinal ischemia is a common cause of visual impairment and blindness. Increased oxidative stress is widely believed to play an important role in retinal ischemic injury. Furthermore, oxidative stress may lead to activation of inflammasomes and caspase-1 and consequently pyroptosis. Sulforaphane, an isothiocyanate, is a precursor of glucosinolate in cruciferous vegetable. Sulforaphane has been shown to protect neural cells in brain ischemia through inhibiting oxidative stress. In this study, we determined if sulforaphane inhibits caspase-1 activation in retinal cells (R28) and improves their viability after exposure to hypoxia.<br />

Methods: The R28 cells were subjected to hypoxia (94.5% N2 / 5% CO2 / 0.5% O2) or non-hypoxic control (95% air / 5% CO2) for 0 - 4 hours. Subsequently, the experimental cultures were treated with sulforaphane (0, 0.25, 0.5, and 1 µM) and cultured in non-hypoxic conditions for 24 hours. The cell viability was determined 24 hours later with neutral red dye uptake assay. The caspase-1 activation was also analyzed by FAM-FLICA TM Caspase-1 Assay Kit.<br />

Results: Hypoxic conditions resulted in R28 cell death and decreased cell viability compared to the cells in the non-hypoxic control. Sulforaphane treatment reduced hypoxia-induced cell death. Caspase-1 activation was increased in hypoxic conditions compared to the non-hypoxic control. Sulforaphane treatment inhibited the caspase-1 activity.<br />

Conclusions: Sulforaphane improves neuro-retinal cell survival under hypoxic conditions through inhibition of caspae-1 activity. These preliminary findings suggest therapeutic value of sulforaphane in retinal ischemia /hypoxic diseases.<br />


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