June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Systemic treatment with xanthohumol protects against light-induced retinal degeneration and maintains retinal redox potential
Author Affiliations & Notes
  • Nathaniel F Henneman
    Ophthalmology, Emory University, Atlanta, Georgia, United States
  • Stephanie Foster
    Ophthalmology, Emory University, Atlanta, Georgia, United States
  • Preston E Girardot
    Ophthalmology, Emory University, Atlanta, Georgia, United States
  • Jeffrey H Boatright
    Ophthalmology, Emory University, Atlanta, Georgia, United States
  • Footnotes
    Commercial Relationships   Nathaniel Henneman, None; Stephanie Foster, None; Preston Girardot, None; Jeffrey Boatright, None
  • Footnotes
    Support  The Abraham and Phyllis Katz Foundation (JHB), VA RR&D C9246C (Atlanta VA Center of Excellence in Vision and Neurocognitive Rehabilitation), VA RR&D C1924P I21RX001924, Research to Prevent Blindness (Emory), NIH NEI P30EY06360 (Emory), NIH NEI R01EY14026 (JHB)
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 5254. doi:
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    • Get Citation

      Nathaniel F Henneman, Stephanie Foster, Preston E Girardot, Jeffrey H Boatright; Systemic treatment with xanthohumol protects against light-induced retinal degeneration and maintains retinal redox potential. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5254.

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

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Abstract

Purpose : The prenylated flavonoid xanthohumol (XN), a constituent of hops, is protective in rodent models of stroke. Here we investigated whether systemic delivery of XN similarly protects in a mouse model of light-induced retinal degeneration (LIRD) and whether such treatment maintains the redox potential of the retina.

Methods : 129SV mice were injected with XN (0.8 mg/kg) or vehicle (4 PBS: 1 ethanol: 1 cremophor) and dilated with 0.1% atropine prior to exposure to 50 or 50,000 lux white light for 4 h. Four weeks after light exposure, function was assessed by electroretinogram (ERG) and optokinetic tracking (OKT) after which mice were sacrificed and retinal morphology assessed. For retinal redox measurement, mice were sacrificed after 2 h of light exposure and retinas analyzed by HPLC for glutathione (GSH), glutathione disulfide (GSSG), cysteine (CYS), and cystine (CYYS).

Results : Mean ERG a- and b-wave amplitudes were significantly higher in toxic-light exposed mice treated with XN versus vehicle (416+63 and 187+48 uV+SEM; 2-way ANOVA/SNK, p<0.001). Acuity was also preserved (OKT cycles per degree+SEM; ANOVA/SNK, p<0.05). XN treatment preserved redox potential in mice exposed to toxic light, with CYSS redox potentials of -52.71+5.13 and -27.15+2.20 and GSSG redox of -141.97+2.47 and -127.21+1.04 mV + SEM, XN versus vehicle, respectively; 1-way ANOVA/SNK, p<0.05. Outer nuclear layer counts showed significant preservation of ONL nuclei with 71.34+25.4 and 176.1+ 19.95 vehicle versus XN, respectively; 1-way ANOVA/SNK, p<0.05.

Conclusions : Toxic light exposure is thought to cause retinal degeneration by increasing oxidative damage. Here we show that XN treatment protects against LIRD, possibly by maintaining retinal CYSS and GSSG redox potential. Though further study is needed, XN may be acting as an antioxidant response inducer as opposed to a direct antioxidant.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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