Neuroprotective effects of cyclosporine A deserve more study

April 25, 2014

Cyclosporine A (CSA) protects retinal ganglion cells (RGCs) against glutamate-induced excitotoxicty and should be tested to see whether its neuroprotective properties will work against RGC disorders, researchers recently reported

Cyclosporine A (CSA) protects retinal ganglion cells (RGCs) against glutamate-induced excitotoxicty and should be tested to see whether its neuroprotective properties will work against RGC disorders, researchers writing in the Journal of Glaucoma say.

The investigators stressed RGC-5 cells with 10 mM glutamate for 24 hours, sometimes adding the immunosuppressive drug (1, 3, 6, or 9 μg/mL) to the medium. They used MTS assay to study cell viability and crystal violet staining to examine cell density, and used caspase 3/7 activity and Annexin V+/PI− flow cytometry to look at apoptosis induction.

They found that RGC-5 cells incubated with 10 mM glutamate for 24 hours had a 3.1-fold decrease in overall cell viability and a 3.4-fold decrease in cell density compared with controls. Adding 9 μg/mL of CSA to 10 mM glutamate caused a 2.7-fold increase in overall cell viability and a 2.5-fold increase in cell density compared with RGC-5 cells treated only with 10 mM glutamate. Also, it significantly reduced caspase 3/7 activity by 1.3-fold and the amount of Annexin V+/PI– cells by 2.8-fold compared with RGC-5 cells incubated with 10 mM glutamate by itself.

"The neuroprotective effect of CSA dose-dependently decreased with lower concentrations," the researchers wrote.

To read the abstract of the study, click here.