OBJECTIVE: To investigate the protective effects of melatonin on the retinal pigment epithelium (RPE) against oxidative damage induced by hydrogen dioxide (H2O2) and its mechanism. METHODS: The RPE cells were seeded and divided into normal control group, oxidative damage group and the treatment group (treated with melatonin at the concentration of 1 x 10(-7) mol/L, 1 x 10(-6) mol/L, 1 x 10(-5) mol/L and 1 x 10(-4) mol/L). The model of oxidative damage on the RPE cells was established by culturing the RPE cells with H2O2 at the concentration of 600 micromol/L for 1 hour in vitro. The cell viability of RPE cells was detected by the methyl thiazolyl tetrazolium (MTT) method. The degree of oxidative damage was evaluated by detecting the superoxide dismutase (SOD) and maleic dialdehyde (MDA). Apoptosis was detected qualitatively using the DNA Ladders electrophoretic method, and quantitatively using the Annexin V-FITC/PI double staining flow cytometry. RESULTS: Compared with normal control group, the oxidative damage group had low cell viability, low SOD and high MDA contents, and high apoptosis rate (t = 2.25, 39.50, 68.42; P < 0.05). Compared with oxidative damage group, the treatment group had high cell viability, high SOD and low MDA contents, and low apoptosis rate (P < 0.05). CONCLUSIONS: Melatonin has a protective effect on the RPE against oxidative damage induced by H2O2. The mechanism may involve in reinforcing the cell viability, strengthening the activity of antioxidase, and reducing the apoptosis.
OBJECTIVE: To investigate the protective effects of melatonin on the retinal pigment epithelium (RPE) against oxidative damage induced by hydrogen dioxide (H2O2) and its mechanism. METHODS: The RPE cells were seeded and divided into normal control group, oxidative damage group and the treatment group (treated with melatonin at the concentration of 1 x 10(-7) mol/L, 1 x 10(-6) mol/L, 1 x 10(-5) mol/L and 1 x 10(-4) mol/L). The model of oxidative damage on the RPE cells was established by culturing the RPE cells with H2O2 at the concentration of 600 micromol/L for 1 hour in vitro. The cell viability of RPE cells was detected by the methyl thiazolyl tetrazolium (MTT) method. The degree of oxidative damage was evaluated by detecting the superoxide dismutase (SOD) and maleic dialdehyde (MDA). Apoptosis was detected qualitatively using the DNA Ladders electrophoretic method, and quantitatively using the Annexin V-FITC/PI double staining flow cytometry. RESULTS: Compared with normal control group, the oxidative damage group had low cell viability, low SOD and high MDA contents, and high apoptosis rate (t = 2.25, 39.50, 68.42; P < 0.05). Compared with oxidative damage group, the treatment group had high cell viability, high SOD and low MDA contents, and low apoptosis rate (P < 0.05). CONCLUSIONS:Melatonin has a protective effect on the RPE against oxidative damage induced by H2O2. The mechanism may involve in reinforcing the cell viability, strengthening the activity of antioxidase, and reducing the apoptosis.