June 2015
Volume 56, Issue 7
ARVO Annual Meeting Abstract  |   June 2015
The Nrf-2 activator sulforaphane protects retinal cells from oxidative stress induced retinal injury
Author Affiliations & Notes
  • Chang-Hao Yang
    Ophthalmology, National Taiwan Univ Hospital, Taipei, Taiwan
  • Chung-May Yang
    Ophthalmology, National Taiwan Univ Hospital, Taipei, Taiwan
  • Hao-Yun Chang
    Ophthalmology, National Taiwan Univ Hospital, Taipei, Taiwan
  • Footnotes
    Commercial Relationships Chang-Hao Yang, None; Chung-May Yang, None; Hao-Yun Chang, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 4232. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Chang-Hao Yang, Chung-May Yang, Hao-Yun Chang; The Nrf-2 activator sulforaphane protects retinal cells from oxidative stress induced retinal injury. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4232.

      Download citation file:

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

  • Supplements

Purpose: Sulforaphane, a natural isothiocynate presented in cruciferous vegetables, is known as activator of transcription factor Nrf2 which activates genes encoding for antioxidative enzymes. In this study, we evaluate the effect of sulforaphane to protect the retina cells in vitro and retina function in vivo.

Methods: ARPE-19 cells was pretreated with sulforaphane following by adding tert-butyl hydroperoxide. Cell viability was evaluated by MTT assay. ROS production and mitochondrial dysfunction were measured by ROS assay and JC-1 Mitochondrial Membrane Potential Assay, respectively. Antioxidative enzymes (HO-1, GR, GPx1, NQO1) and proinflammatory mediators (ICAM-1, MCP-1) were quantified by PCR and western analysis. For in vivo study, Sprague-Dawley rats were randomized to receive saline, low-dose or high-dose sulforaphane treatment before ischemia reperfusion (IR) injury. ERG was used to measure retinal function. ROS production with retina was evaluated. EMSA were used to check the activation of Nrf2 and NF-kB in retinal cells.

Results: Pretreatment with sulforaphane dramatically increased cell survival after exposure to oxidative stress, significantly decreased cell production of reactive oxygen species, and attenuated the mitochondrial dysfunction. Sulforaphane successfully induced anti-oxidant proteins HO-1, GR, GPx1, and NQO1 in a dose-depentend manner by activated Nrf2. Sulforaphane reduced the elevation of proinfammatory mediators ICAM-1 and MCP-1, by decreased the NF-kB activation. In vivo experiment demonstrated sulforaphane significantly preserved the ERG b-wave after IR injury on rat’s retina. Pretreatment of sulforaphane diminished ROS production in retina after IR injury. EMSA study showed NF-kB was deactivated and Nrf2 was activated by sulforaphane in rat’s retina.

Conclusions: Treatment of ARPE 19 cell with sulforaphane effectively protected cells against oxidative stress by activated the Nrf2-dependent proteins to increase the anti-oxidative effect. Sulforaphane also preserved the retina function after IR injury in vivo. These results supported that sulforaphane had the cytoprotective effect against oxidative stress and may be useful in combating human acute retinal IR injury.


This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.