Intense exposure to light, robust metabolic activity, and high oxygen tension render the human eye particularly vulnerable to oxidative damage and the list of ophthalmological disorders implicating reactive oxygen species is rapidly expanding. The present study involves reducing or preventing damage to the cornea resulting from oxidative stress by up-regulating the SIRT1 level. Data was collected from the tissue culture experiments using the human corneal cell line (2.040 pRSV-T) as a model of corneal tissue and the chemical compounds (SRT1720, SRT1460, and resveratrol) as SIRT1 activators. The results indicate that SRT1720 eliminated cellular morphological changes related to oxidative stress by H2O2 treatment and increased cell proliferation under oxidative stress. Results indicated that targeting oxidative damage of the cornea by SRT1720 is therapeutically beneficial.
Key words: 2.040 pRSV-T cell line, MTS, SRT1460, SRT1720.
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