PURPOSE: To investigate whether caffeic acid phenethyl ester (CAPE) has a protective effect on retinal ischemia/reperfusion (I/R) injury in rats, and to determine the possible antioxidant mechanisms. METHODS: Seventy-six female Wistar rats were randomized evenly into Sham, I/R injury model (M group), model plus vehicle (MV), and model plus CAPE (MC) groups. Retinal ischemia/reperfusion injury was induced by increasing the intraocular pressure to 110 mmHg for 60 min. Rats in the MV and MC groups were injected with vehicle and CAPE (10 µmol/kg i.p.), respectively, before reperfusion and once a day for one or seven days after I/R. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in the retinal tissues were determined 24 hr after I/R. Retinal cells apoptosis was detected 24 hr after I/R injury by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP nick-end labeling staining. On day 7 after reperfusion, the electroretinogram (ERG) was recorded, and the retinal histology was examined and quantified using light microscopy. RESULTS: CAPE significantly decreased the MDA levels and increased the activities of SOD, GSH-Px, and CAT in the retina compared with the ischemia group (p< 0.05). CAPE attenuated the I/R-induced apoptosis of retinal cells in the inner nuclear and ganglion cells of the rat retina. CAPE also suppressed the I/R-induced reduction in the a- and b-wave amplitudes of the ERG (p<0.05). The thickness of the entire retina, inner nuclear layer, and inner plexiform layer and the number of cells in the ganglion cell layer in the MC group were significantly greater than those in the M group (p<0.05). CONCLUSIONS: CAPE can protect the rat retina from I/R injury by enhancing the antioxidation ability and inhibiting the apoptosis of retinal cells, which suggests that CAPE is potentially useful for treating I/R-induced eye disorders.
PURPOSE: To investigate whether caffeic acid phenethyl ester (CAPE) has a protective effect on retinal ischemia/reperfusion (I/R) injury in rats, and to determine the possible antioxidant mechanisms. METHODS: Seventy-six female Wistar rats were randomized evenly into Sham, I/R injury model (M group), model plus vehicle (MV), and model plus CAPE (MC) groups. Retinal ischemia/reperfusion injury was induced by increasing the intraocular pressure to 110 mmHg for 60 min. Rats in the MV and MC groups were injected with vehicle and CAPE (10 µmol/kg i.p.), respectively, before reperfusion and once a day for one or seven days after I/R. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in the retinal tissues were determined 24 hr after I/R. Retinal cells apoptosis was detected 24 hr after I/R injury by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP nick-end labeling staining. On day 7 after reperfusion, the electroretinogram (ERG) was recorded, and the retinal histology was examined and quantified using light microscopy. RESULTS:CAPE significantly decreased the MDA levels and increased the activities of SOD, GSH-Px, and CAT in the retina compared with the ischemia group (p< 0.05). CAPE attenuated the I/R-induced apoptosis of retinal cells in the inner nuclear and ganglion cells of the rat retina. CAPE also suppressed the I/R-induced reduction in the a- and b-wave amplitudes of the ERG (p<0.05). The thickness of the entire retina, inner nuclear layer, and inner plexiform layer and the number of cells in the ganglion cell layer in the MC group were significantly greater than those in the M group (p<0.05). CONCLUSIONS:CAPE can protect the rat retina from I/R injury by enhancing the antioxidation ability and inhibiting the apoptosis of retinal cells, which suggests that CAPE is potentially useful for treating I/R-induced eye disorders.