May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Estrogen Mediates Oxidative Stress and Protects Retinal Neurons Against Ischemic Injury in Rats
Author Affiliations & Notes
  • P.–H. Peng
    Ophthalmology, Shin–Kong Memorial Hosp, Taipei, Taiwan Republic of China
  • M.–L. Ko
    Ophthalmology, Hsin–Chu Hospital, Hsin–Chu, Taiwan Republic of China
  • C.–F. Chen
    Physiology, National Taiwan University, Taipei, Taiwan Republic of China
  • Footnotes
    Commercial Relationships  P. Peng, None; M. Ko, None; C. Chen, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 158. doi:
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      P.–H. Peng, M.–L. Ko, C.–F. Chen; Estrogen Mediates Oxidative Stress and Protects Retinal Neurons Against Ischemic Injury in Rats . Invest. Ophthalmol. Vis. Sci. 2005;46(13):158.

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

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Abstract: : Purpose: To examine the protective effect of 17ß–estradiol on retina ischemia–reperfusion injury and the possible underlying mechanisms. Methods: Female Wistar rats were divided into normal, ovariectomized, and exogenous supplement of estrogen groups. 17ß–estradiol was administrated 2h before experiment. 60–minute transient ischemia was induced in these three groups unilaterally in the rat eye by cannulating the anterior chamber and raising the intraocular pressure over systemic blood pressure. ICI182780, the antagonist of estrogen receptor blocker, was injected intravitreally. The protective effects were evaluated by the cell counts of pre–labeling retinal ganglion cells (RGC). The levels of apoptosis were determined by using TdT–dUTP terminated nick–end labeling (TUNEL) method and western blot of active–caspase 3. Lipid peroxides and the activity of superoxide dismutase (SOD) to reflect the oxidative status were measured by spectrophotometry. The expressions of neuronal nitric oxide synthase (nNOS) and nicotinamidne adenine dinucleotide phosphate (NADPH) of retina were observed by immunohistochemistry. Results: Decreased numbers of RGC and cell death by apoptosis were noted after ischemia. The density of RGC also reduced after ovariectomy. Estrogen treated eyes preserved more RGC and attenuated apoptosis. In addition, ischemia induced elevating lipid membrane oxidation and decreasing SOD activity were reversed by estrogen. Treated with estrogen minimized nNOS and NADPH positively stained cells after ischemia as well. Estrogen receptor blocker ICI182780 has abolished the effect of estrogen in some aspects. Conclusions: Pre–treated with estrogen significantly protected rat retina against ischemia–reperfusion injury, especially cell death through apoptotic process. Acting as antioxidant was indicated from the results of our study. Estrogen receptor dependent pathway might play some roles in this protective effect.

Keywords: cell death/apoptosis • neuroprotection • antioxidants 

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