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Abstract

Melatonin’s Antioxidative Characteristic in Human Aging Retinal Pigment Epithelial Cells

Author(s): Govand SH Tawfeeq* and Ismail S Kakey
Department of Clinical Analysis, College of Pharmacy, Hawler Medical University, Erbil, Kurdistan Region, Iraq, 1Department of Biology, Faculty of Science and Health, Koya University, Koya KOY45, Kurdistan Region, F. R. Iraq

Correspondence Address:
Govand SH Tawfeeq, Department of Clinical Analysis, College of Pharmacy, Hawler Medical University, Erbil, Kurdistan Region, Iraq, E-mail: govand.tawfeeq@hmu.edu.krd


In this study, the antioxidative effect of melatonin was investigated in aging retinal pigment epithelial cells in vitro. The objective of this study is to explore the administration of melatonin pharmacological doses for the prevention of aging symptoms.Specific concentrations of melatonin (20 µM, 40 µM and 80 µM) were used to treat hydrogen peroxide-induced aging retinal pigment epithelial cells and flow cytometry was employed to examine retinal pigment epithelial cell apoptosis. A specific probe was utilized to detect the intracellular reactive oxygen species concentration and apoptosis-associated proteins were detected in real-time polymerase chain reaction. Commercially available assay kits detected the expression of oxidative biomarkers, superoxide dismutase, malondialdehyde and glutathione.In comparison to normal cells, the aging retinal pigment epithelial cell model had lower cell viability, higher apoptosis rates and a more severe oxidation status. Melatonin increased cell viability while lowering apoptosis and oxidative stress. It influenced the expression of apoptosis-related proteins as well as oxidative stress indicators. Finally, treatment with melatonin was able to regulate proliferation, oxidative stress and apoptosis in aging retinal pigment epithelial cells.The application of melatonin may be a novel strategy to protect against age-related changes in age-related macular degeneration. Melatonin has protective effects against hydrogen peroxide-induced retinal cell death. It inhibits hydrogen peroxide-induced retinal pigment epithelial cell damage and decreases the apoptosis rate.

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