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Miin Roh, Yusuke Murakami, Aristomenis Thanos, Demetrios Vavvas, Joan W. Miller; Edaravone, A Ros Scavenger, Ameliorates Photoreceptor Apoptosis After Experimental Retinal Detachment. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4914.
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To investigate whether edaravone (3-methyl1-phenyl-2-pyrazolin-5-one), a free radical scavenger is neuroprotective against photereceptor death in a rat model of retinal detachment (RD).
RD was induced in adult Brown Norway rats by subretinal injection of sodium hyaluronate. Edaravone (3 mg/kg, 5 mg/kg, 10 mg/kg) or physiologic saline were administered intraperitoneally once a day until sacrifice on day 3 or 5. Oxidative stress in the retina was assessed by 4-hydroxynonenal staining or ELISA for protein carbonyl content. Photoreceptor death was assessed by TUNEL and measurement of the outer nuclear layer thickness . Western blot analysis and caspase activity assays were performed. Inflammatory cytokine secretion and inflammatory cell infiltration were evaluated by ELISA and immunostaining, respectively.
RD resulted in increased generation of ROS. Treatment with 5 mg/kg edaravone significantly reduced ROS level along with decrease in TUNEL positive cells in the photoreceptor layer. Caspase assay also confirmed decreased activation of caspases -3,-,8, and -9 in RD treated with edaravone. The level of the anti-apoptotic Bcl-2 was increased in detached retinas after edaravone treatment, whereas the levels of the stress-activated p-ERK1/2 were decreased. Additionally, edaravone treatment resulted in a significant decrease in the levels of TNF-α, MCP-1 and macrophage infiltration.
Oxidative stress plays an important role in the photoreceptor apoptosis after RD. Edaravone treatment may aid in preventing photoreceptor apoptosis following RD by suppressing ROS-induced photoreceptor damage.
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