Purpose This study was to determine whether Crepidiastrum denticulatum, is effective at blunting the negative influence of 1-buthionine-(S,R)-sulfoximine (BSO, 0.5 mM) plus glutamate (10 mM) in transformed retinal ganglion cells (RGC-5) and of N-methyl-D-aspartate (NMDA) to the rat retina. Methods RGC-5 cells in culture were given negative insult such as BSO plus glutamate for 24 hours, after which cell survival were tested. Reactive oxygen species (ROS) quantification was performed by 2΄,7΄-dichlorodihydrofluorescein diacetate and dihydroethidium. Apoptotic cell death was measured by propidium iodide (PI)/Hoechst 33342 double staining and western blot analysis. NMDA-induced retinal damage in vivo was tested by hematoxylin-eosin staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL) staining. The lipid peroxidation was tested by amount of formation for thiobarbituric acid reactive species. Results The ethanol extract of C. denticulatum (EECD) significantly attenuated RGC-5 cells death caused by BSO plus glutamate. Treatment of the RGC-5 cells with EECD reduced the ROS caused by various radical species such as H2O2, OH• or O2•-. The up (cleaved PARP and cleaved caspase-3) and down (Bcl-2) regulations of apoptotic proteins caused by BSO plus glutamate were significantly blunted by EECD. EECD protected the negative influence of NMDA on the retinas of rats of the thinning of the inner plexiform layer (IPL) and of the increased TUNEL in positive ganglion cells in the ganglion cell layer. Chlorogenic acid and 3,5-dicaffeoylquinic acid were found to be major components of EECD. Conclusion EECD could be promoted as a potential neuroprotective agent for glaucoma against oxidative stress.
