title: Protective effects of caffeic acid phenethyl ester on retinal ischemia/reperfusion injury in rats.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Ophthalmology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China.
authors.forename: Yuhua
authors.initials: Y
authors.lastname: Shi
authors.forename: Xingwei
authors.initials: X
authors.lastname: Wu
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Gong
authors.forename: Yating
authors.initials: Y
authors.lastname: Qiu
authors.forename: Hongmei
authors.initials: H
authors.lastname: Zhang
authors.forename: Zhenping
authors.initials: Z
authors.lastname: Huang
authors.forename: Kaiming
authors.initials: K
authors.lastname: Su
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002109:Caffeic Acids / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D004596:Electroretinography; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D020287:In Situ Nick-End Labeling; D066298:In Vitro Techniques; D008315:Malondialdehyde / Q000037:antagonists & inhibitors; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D010626:Phenylethyl Alcohol / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D012160:Retina / Q000187:drug effects / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D012171:Retinal Vessels / Q000187:drug effects*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D002109:Caffeic Acids; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; C055494:caffeic acid phenethyl ester; D010626:Phenylethyl Alcohol