Abstract
Purpose: :
Multiple pathologic processes are involved in neovascular age related macular degeneration (AMD). Current therapies focus on the control of active neovascularisation. There is increasing interest in incorporating therapies that block other pathophysiologic processes not directly related to neovascularisation such as inflammation to preserve long-term vision. Minocycline, a semisynthetic tetracycline has been shown to have immunomodulatory effects on the inflammatory process. Minocycline is proposed as an anti-inflammatory agent to protect retinal pigment epithelial cells. This study investigated the effect of Minocycline on oxidative stress induced RPE cell damage.
Methods: :
ARPE-19 cells were maintained in Dulbecco’s modified Eagle medium supplemented with glutamine, penicillin, streptomycin, amphotericin and 10% fetal calf serum. Cells were exposed to hydrogen peroxide as a source of oxidative stress, then exposed to varying concentrations of Minocycline. Cell counts for viability were performed after exposure to acute and chronic oxidative stress conditions and Minocycline exposure.
Results: :
Comparison of cell count viability data with the Mann Whitney test showed no difference between acute oxidative stress exposure alone and with Minocycline (p=0.11)After chronic oxidative stress exposure cell viability counts increased significantly after exposure to Minocycline (p=0.04)
Conclusions: :
The results suggest minocycline protects retinal pigment epithelial cells from the effects of chronic oxidative stress in culture and supports the potential role of Minocycline as an adjuvant treatment for neovascular AMD.
Keywords: age-related macular degeneration • inflammation • retinal pigment epithelium