title: Protective effects of catalase on retinal ischemia/reperfusion injury in rats.
abstract: Retinal ischemia/reperfusion (I/R) injury causes profound tissue damage, especially retinal ganglion cell (RGC) death. The aims of the study were to investigate whether catalase (CAT) has a neuroprotective effect on RGC after I/R injury in rats, and to determine the possible antioxidant mechanism. Wistar female rats were randonmized into four groups: normal control group (Control group), retinal I/R with vehicle group (I/R with vehicle group), retinal I/R with AAV-CAT group (I/R with AAV-CAT group), and normal retina with AAV-CAT group (normal with AAV-CAT group). One eye of each rat was pretreated with recombinant adeno-associated virus containing catalase gene (I/R with AAV-CAT group or normal with AAV-CAT group) and recombinant adeno-associated virus containing GFP gene (I/R with vehicle group) by intravitreal injection 21 days before initiation of I/R injury. Retinal I/R injury was induced by elevating intraocular pressure to 100mmHg for 1h. The number of RGC and inner plexiform layer (IPL) thickness were measured by fluorogold retrograde labeling and hematoxylin and eosin staining at 6h, 24h, 72 h and 5d after injury. Hydrogen peroxide (H(2)O(2)), the number of RGC, IPL thickness, malondialdehyde(MDA), 8-hydroxy-2-deoxyguanosine (8-OHdG), CAT activity and nitrotyrosine were measured by fluorescence staining, immunohistochemistry and enzyme-linked immunosorbent assay analysis at 5 days after injury. Electroretinographic (ERG) evaluation was also used. Pretreatment of AAV-CAT significantly decreased the levels of H(2)O(2), MDA, 8-OHdG and nitrotyrosine, increased the catalase activity, and prevented the reduction of a- and b- waves in the I/R with AAV-CAT group compare with the I/R with vehicle group (p<0.01). Catalase attenuated the I/R-induced damage of RGC and IPL and retinal function. Therefore, catalase can protect the rat retina from I/R-induced injury by enhancing the antioxidative ability and reducing oxidative stress, which suggests that catalase may be relevant for the neuroprotection of inner retina from I/R-related diseases.
authors.affiliation: Department of Ophthalmology, Second Xiangya Hospital, Central South University, 139 Renming Middle Road, Changsha Hunan Province 410011, PR China.
authors.forename: Baihua
authors.initials: B
authors.lastname: Chen
authors.forename: Luosheng
authors.initials: L
authors.lastname: Tang
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D000975:Antioxidants; D017209:Apoptosis / Q000502:physiology; D002374:Catalase / Q000235:genetics*; D002452:Cell Count; D002470:Cell Survival; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D000229:Dependovirus / Q000235:genetics*; D004596:Electroretinography; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D015316:Genetic Therapy; D005822:Genetic Vectors; D007150:Immunohistochemistry; D008315:Malondialdehyde / Q000378:metabolism; D018696:Neuroprotective Agents; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D012160:Retina / Q000502:physiology; D012164:Retinal Diseases / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D012165:Retinal Ganglion Cells / Q000378:metabolism / Q000473:pathology*; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism
chemical_list: D000975:Antioxidants; D018696:Neuroprotective Agents; C002744:3-nitrotyrosine; D014443:Tyrosine; D008315:Malondialdehyde; D000080242:8-Hydroxy-2'-Deoxyguanosine; D002374:Catalase; D003849:Deoxyguanosine