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Yanhong Wei, Junsong Gong, Takeshi Yoshida, Rajesh Thimmulappa, Shyam Biswal, Elia J. Duh; Nrf2 Modulates Oxidative Stress, Inflammation, and Neurovascular Injury in Retinal Ischemia-reperfusion. Invest. Ophthalmol. Vis. Sci. 2011;52(14):6060.
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Retinal ischemia-reperfusion (I/R) involves extensive increase in reactive oxygen species as well as pro-inflammatory changes, with subsequent neuronal and vascular degeneration. Nrf2 has a well-known cytoprotective role in many tissues, although its function in the retina is less clear. The purpose of this study is to investigate the possible role of Nrf2 in retinal I/R injury using Nrf2-deficient mice.
Retinal I/R injury was induced by elevating the intraocular pressure (IOP), and reperfusion was established immediately afterward. Dihydroethidium (DHE) staining and biochemical assay using lucigenin were used for superoxide measurement. Histological analysis, cell count in the ganglion cell layer, and apoptotic DNA cleavage ELISA were performed after 48 hours of I/R injury. Inflammatory gene expression was assessed by real-time PCR. Capillary degeneration was quantified in retinas 8 days after I/R.
I/R resulted in an increase in retinal levels of superoxide and pro-inflammatory mediators in Nrf2 +/+ mice, an effect which was accentuated in Nrf2 -/- mice. Leukocyte infiltration of the retina and vitreous, loss of cells in the ganglion cell layer, and retinal capillary degeneration were markedly accentuated by I/R in Nrf2 -/- mice as compared to wild-type.
These studies indicate that Nrf2 is an important factor in modulating the retinal response to ischemia-reperfusion injury.
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