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Wei Huang, Guorong Li, Jianming Qiu, Pedro Gonzalez, Pratap Challa; The Protective effects of Resveratrol in Experimental Retinal Detachment. Invest. Ophthalmol. Vis. Sci. 2013;54(15):4198.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate whether Resveratrol, a potent antioxidant and small molecule activator of the FoxO pathway, would be neuroprotective against photoreceptor cell death in a rodent model of retinal detachment (RD).
Retinal detachment was created in adult Brown Norway rats by subretinal injection of sodium hyaluronate. The animals were treated daily with vehicle, Resveratrol (20mg/kg) intraperitoneal injection. Photoreceptor death was assessed by counting the number of apoptotic cells with TdT-dUTP terminal nick-end labeling (TUNEL) and measurement of the outer nuclear layer (ONL) thickness 3 days after RD. Changes in expression of FoxO1A, FoxO3A, and FoxO4 were analyzed by western blot. The activity of Caspase 3, Caspase 9, Spectrin and their cleavage forms were studied.
Three days after RD, Caspase 3, Caspase 9 were activated. There was no activation of a 120 kDa form of Spectrin, Calpain specific substrates, detected. Resveratrol treatment increases FoxO1A, FoxO3A, and FoxO4 protein, a family of transcription factors known to regulate the defense against reactive oxygen species, expression in RD retina. Resveratrol treatment partially blocks Caspases activation. Resveratrol significantly decreases the number of TUNEL-positive cells and preserves ONL thickness in both systemic only and systemic with local treatment group.
Resveratrol has potential be used as a novel therapeutic agent for preventing vision loss in diseases that are characterized by photoreceptor detachment.
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