Pharmacological protection of retinal pigmented epithelial cells by sulindac involves PPAR-α

Oxidative stress-induced damage to retinal pigmented epithelial (RPE) cells is implicated in the progression of age-related macular degeneration (AMD), which is one of the primary causes of vision loss in the elderly. The present studies show that sulindac, a known nonsteroidal antiinflammatory drug, can protect an established RPE cell line, low-passage human fetal RPE, and polarized primary human fetal RPE cells against oxidative damage. The results with the RPE cell line indicate that the protective response is similar to that seen with ischemic preconditioning. Our results suggest that preventing oxidative damage in RPE cells by this drug-induced protective mechanism could be an inexpensive and relatively nontoxic therapeutic approach for AMD treatment.