Abstract
Purpose: :
The loss of neuronal cells under cell stress is connected to a decrease of intracellular calcium. Memantine inhibits the glutamate induced calcium decrease blocking the NMDA–receptor. The NMDA–antagonist is used in the treatment of Alzheimer`s disease. The aim of our study is to examine protective effects of memantine on RGC (retinal ganglion cells) after methylglyoxal treatment. RGC are known to be the critical site for degenerative processes in diabetic retinopathy or glaucoma.
Methods: :
Retinal cell lines (R28) were incubated with MG for 5 hours. Memantine was added 0–30 min before MG–damaging. Necrotic and apototic cells were measured by specific flowcytometric assays. Changes in mitochondrial potential were analyzed by JC 1–fluorescence. Differences between the groups were compared using the chi–square test. P values < 0,05 were considered to be significant.
Results: :
We found a substantial reduction in apoptosis (26%) (p<0.05) in memantine treated R28 cultures compared to the contol group . There were no differences in the number of necrotic cells between memantine culture and control goup. Furthermore statistically significant differences could be observed in the concentration of memantine and the point of time it was added. No reduction in apoptosis was seen by simultaneous dose of memantine and MG.
Conclusions: :
Our results show protective effects of memantine on RGC. In the future further in vivo studies are planned to verify these protective effects.
Keywords: neuroprotection • ganglion cells • pharmacology