Abstract
Abstract: :
Purpose: To determine the neuropotective effect of Ca2+ channel blockers, lomerizine, nimodipine, and iganidipine on hypoxic damage of purified rat retinal ganglion cells. Methods: Retinal ganglion cell (RGC) cultures purified with two–step immunopanning method from fetal rat retina were used. RGCs were cultured under hypoxia (5% O2, 5%CO2, 37°C) for 12 hours with lomerizine (0.01–1µM), nimodipine(0.01–1µM), or iganidipine (0.01–1µM). Cell viability of RGC cultured with these 3 durgs was assessed by calceinAM staining and compared to that of non–treated control culture. Intracellar Ca2+ concentration was also assessed using Ca2+ imaging device. Results: The viability of control culture after 12 hours of hypoxia was 44.0%+/–4.5%. The viability of all treated cultures increased in a dose–dependent manner; lomerizine (0.01µM:43.7%, 0.1µM:49.1%, 1µM:57.1%, n=7), nimodipine (0.01µM:49.3%, 0.1µM:53.0%, 0.01µM:55.4%, n=7), and iganidipine (0.01µM:50.0%, 0.1µM:54.5%, 0.01µM:54.5%, n=7). The viability of all treated cells was significantly increased compared to that of control cells (p<0.05). Intracellar Ca2+ concentration in treated cells was lower than that in non–treated cells. Conclusions: These results suggest that lomerizine, nimodipine, and iganidipine can directly protect RGC against hypoxia. Ca2+ channel blockers may be effective in the prevention of hypoxia–induced RGC death partly through a mechanism unrelated to their vasodilator effect.
Keywords: calcium • neuroprotection • ganglion cells