title: Monosialoganglioside GM1 reduces ischemia--reperfusion-induced injury in the rat retina.
abstract: OBJECTIVE
  Gangliosides are normal components of cell membranes, contribute to structural rigidity and membrane function, and have been shown to protect against various insults to the brain. This study evaluates the effect of exogenously administered monosialoganglioside GM1 on retinal damage induced by transient retinal ischemia and reperfusion.
  
  
  METHODS
  Retinal ischemia was induced unilaterally in Long Evans rats by increasing intraocular pressure to 160 mm Hg for 60 minutes. GM1 (30 mg/kg, intraperitoneally) or buffer controls were administered at 48 hours, and 15 minutes before ischemia, and survival time after ischemia was either 8 or 15 days. The degree of retinal damage was assessed by histopathologic study according to Hughes' quantification of ischemic damage.
  
  
  RESULTS
  Retinal ischemia led to significant reductions in thickness and cell number, principally in the inner retinal layers (30% to 80%), and to a lesser extent in the outer retinal layers (18% to 42%). Pretreatment with intraperitoneally injected monosialoganglioside GM1 conferred significant protection against retinal ischemic damage either 8 or 15 days after ischemic survival time. After 8 days reperfusion, the ischemic-induced loss in overall retinal thickness was reduced by 70%, and those of the inner nuclear and plexiform layers were reduced by 77% and 44%, respectively. Ischemic-induced ganglion cell, inner nuclear, and outer nuclear layer cell density losses were reduced by 45%, 40%, and 57%, respectively. After 15 days of reperfusion, approximately the same statistically significant differences could be observed in comparison with the 15-day ischemic--reperfusion group.
  
  
  CONCLUSIONS
  Monosialoganglioside GM1 protects the rat retina from pressure-induced ischemic injury when administered intraperitoneally 2 days before insult. This protection afforded by GM1 can be observed even after 8 days or 15 days of reperfusion.
authors.affiliation: Department of Ophthalmology, Centre Hospitalo--Universitaire de Nantes, France.
authors.forename: M
authors.initials: M
authors.lastname: Weber
authors.forename: S
authors.initials: S
authors.lastname: Mohand-Said
authors.forename: D
authors.initials: D
authors.lastname: Hicks
authors.forename: H
authors.initials: H
authors.lastname: Dreyfus
authors.forename: J A
authors.initials: JA
authors.lastname: Sahel
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002452:Cell Count; D016923:Cell Death; D004195:Disease Models, Animal; D005677:G(M1) Ganglioside / Q000494:pharmacology / Q000627:therapeutic use*; D007274:Injections, Intraperitoneal; D007511:Ischemia / Q000188:drug therapy / Q000473:pathology; D051381:Rats; D015424:Reperfusion; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000473:pathology; D012160:Retina / Q000187:drug effects / Q000473:pathology; D012161:Retinal Artery / Q000187:drug effects / Q000473:pathology; D012164:Retinal Diseases / Q000188:drug therapy* / Q000473:pathology
chemical_list: D005677:G(M1) Ganglioside