title: Diosmin protects rat retina from ischemia/reperfusion injury.
abstract: OBJECTIVE
  Diosmin, a natural flavone glycoside, possesses antioxidant activity and has been used to alleviate ischemia/reperfusion (I/R) injury. The aim of this study was to clarify whether the administration of diosmin has a protective effect against I/R injury induced using the high intraocular pressure (IOP) model in rat retina, and to determine the possible antioxidant mechanisms involved.
  
  
  METHODS
  Retinal I/R injury was induced in the rats by elevating the IOP to 110 mmHg for 60 min. Diosmin (100 mg/kg) or vehicle solution was administered intragastrically 30 min before the onset of ischemia and then daily after I/R injury until the animals were sacrificed. The levels of malondialdehyde (MDA) and the activities of total-superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in the retinal tissues were determined 24 h after I/R injury. At 7 days post-I/R injury, electroretinograms (ERGs) were recorded, and the density of surviving retinal ganglion cells (RGCs) was estimated by counting retrograde tracer-labeled cells in whole-mounted retinas. Retinal histological changes were also examined and quantified using light microscopy.
  
  
  RESULTS
  Diosmin significantly decreased the MDA levels and increased the activities of T-SOD, GSH-Px, and CAT in the retina of rats compared with the ischemia group (P<0.05), and 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, inner plexiform layer, and outer retinal layer and the number of cells in the ganglion cell layer were significantly less after I/R injury (P<0.05), and diosmin remarkably ameliorated these changes on retinal morphology. Diosmin also attenuated the I/R-induced loss of RGCs of the rat retina (P<0.05).
  
  
  CONCLUSIONS
  Diosmin protected the retina from I/R injury, possibly via a mechanism involving the regulation of oxidative parameters.
authors.affiliation: Department of Ophthalmology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China.
authors.forename: Nianting
authors.initials: N
authors.lastname: Tong
authors.forename: Zhenzhen
authors.initials: Z
authors.lastname: Zhang
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Gong
authors.forename: Lili
authors.initials: L
authors.lastname: Yin
authors.forename: Xingwei
authors.initials: X
authors.lastname: Wu
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000627:therapeutic use*; D002374:Catalase / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D004145:Diosmin / Q000008:administration & dosage / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004596:Electroretinography; D005979:Glutathione Peroxidase / Q000378:metabolism; D007429:Intraocular Pressure / Q000187:drug effects*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009798:Ocular Hypertension / Q000150:complications / Q000188:drug therapy*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000209:etiology / Q000517:prevention & control*; D012160:Retina / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D012165:Retinal Ganglion Cells / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D008315:Malondialdehyde; D004145:Diosmin; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase