Abstract
Purpose: :
Grape seed extract (GSE) is known to be a potent antioxidant. We examined the effect of GSE on oxidative stress-induced cell death in a transformed retinal ganglion cell line, RGC-5.
Methods: :
Staurosporine differentiated RGC-5 (ssdRGC-5) cells, obtained by treatment of RGC-5 cells with 1 µM staurosporine, were incubated with GSE for 2h and then exposed to buthionine sulfoximine (BSO) plus glutamate (B/G) for 24 h. Cell death was detected by LIVE/DEAD viability assay and types of cell death were evaluated using fluorescein isothiocyanate (FITC)-conjugated annexin V/ propidium iodide (PI) staining methods. To investigate the possible underlying mechanism of cell death, we determined caspase-3 activity and the level of reactive oxygen species (ROS) formation.
Results: :
Treatment of ssdRGC-5 cells with B/G increased intracellular ROS and induced apoptosis (not necrosis) with increasing caspase-3 activity. GSE rescued ssdRGC-5 cells from oxidative stress-induced cell death by inhibiting both intracellular ROS production and caspase-3 activation.
Conclusions: :
GSE showed a neuroprotective effect against oxidative stress-induced apoptotic death in ssdRGC-5 cells. This finding suggests that GSE could be a possible candidate for a therapeutic agent in glaucoma treatment.
Keywords: neuroprotection • retinal culture • drug toxicity/drug effects