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X. Liang, F. Chen, H. Zhou, C. Yang, G. Sun, Q. Gao, Y. Luo, J. Ge; SS31 Protects Human RPE Cells From Oxidative Damage and Reduce Laser-Induced Choroidal Neovascularization. Invest. Ophthalmol. Vis. Sci. 2010;51(13):1406.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate whether a new peptide SS31 may protect human retinal pigment epithelial(hRPE) cells from oxidative damage and reduce choroidal neovascularization in mice.
Cultured hRPE cells were pretreated with SS31 for 4 hours followed by treatment with tert-butylhydroperoxide(t-BHP). Reactive oxygen species (ROS) was measured by using H(2)DCF, changes in mitochondrial membrane potential were detected by JC-1 dye, apoptosis was detected by using Annexin V-FITC Kit, malondialdehyde(MDA) level was determined by a method based on the reaction with thiobarbituric acid. Then, five to six-week-old C57BL/6 male mice had laser-induced rupture of Bruch’s membrane at four locations in each right eye. Daily intraperitoneal injections of 1mg/Kg(Group1), 9mg/Kg SS31(Group2) or vehicle(Control) were started the day prior to laser photocoagulation. After one week, the mice were perfused with FITC-dextran and CNV areas were measured on choroidal flat mounts.
Pretreatment of hRPE cells with 1µM SS31 significantly reduced the t-BHP-induced intracellular ROS and MDA level by 46% and 34% respectively, protected against t-BHP-induced decreases in mitochondrial membrane potential, and prevented oxidant-induced cell apoptosis. In vivo study showed the average areas of CNV were 0.013±0.0034 mm2/eye(Control),0.0068±0.0025mm2/eye(Group1), 0.0067±0.0026mm2 /eye(Group2). Compared with the Control group, the average areas of CNV in Group1 and Group2 decreased 47.4% and 48.1% (p<0.01), but there was no significant difference between SS31-treated groups.
These results suggest that SS31 could protect against oxidative damage in hRPE cells and suppress Laser-Induced Choroidal Neovasculari-zation.It could be effective against age-associated increase in oxidative stress and mitochondrial dysfunction in RPE cells, and have clinical utility for treatment of Age-related Macular Degeneration.
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