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AIM:To evaluate the neuroprotective effect of rosuvastatin,in a rat experimental glaucoma model.· METHODS:Ocular hypertension was induced in right eyes of Long-Evans rats(n=30) by cauterization of three episcleral veins.Left eyes were defined as controls.Rats were divided into five groups:oral rosuvastatin,intravitreal rosuvastatin,oral +intravitreal rosuvastatin,intravitreal sham and glaucoma without intervention.Rats were sacrificed at day 14.Retinal ganglion cell(RGC) number was assessed by histopathological analysis.Terminal deoxynucleotidyl transferase-mediated dUTP-nick end-labeling(TUNEL) staining and the expression of glial fibrillary acidic protein(GFAP) in RGC layer was also examined.· RESULTS:A significant intraocular pressure(IOP)elevation was seen(P=0.002).Elevated IOP resulted in a significant decrease in number of RGCs in group 5(70.33±8.2 cells/mm~2) when compared with controls(92.50±13.72 cells/mm~2;P=0.03).The RGC number in group 1(92.4±7.3 cells/mm~2) was significantly higher than group 5(P=0.03).The numbers of RGC in groups 2,3(57.3±8.2 cells/mm~2,60.5±12.9 cells/mm~2) were comparable with that of group 5(P=0.18 and P=0.31).The apoptosis rates with TUNEL staining were also parallel to RGC number.Animals with experimentally induced glaucoma showed an increase in retinal GFAP immunoreactivity.· CONCLUSION:Decrease in RGC loss and apoptosis suggest the neuroprotective potential of oral rosuvastatin treatment in a rat model of ocular hypertension.However intravitreal rosuvastatin showed a contrary effect and further studies are required.
AIM: To evaluate the neuroprotective effect of rosuvastatin, in a rat experimental glaucoma model. · METHODS: Ocular hypertension was induced in right eyes of Long-Evans rats (n = 30) by cauterization of three episcleral veins. Left eyes were defined as controls . Rats were divided into five groups: oral rosuvastatin, intravitreal rosuvastatin, oral + intravitreal rosuvastatin, intravitreal sham and glaucoma without intervention. Rats were sacrificed at day 14. Retinal ganglion cell (RGC) number was assessed by histopathological analysis. Termina deoxynucleotidyl transferase- mediated dUTP-nick end-labeling (TUNEL) staining and the expression of glial fibrillary acidic protein (GFAP) in RGC layer was also examined. RESULTS: A significant intraocular pressure (IOP) elevation was seen (P = 0.002) resulted in a significant decrease in the number of RGCs in group 5 (70.33 ± 8.2 cells / mm ~ 2) when compared with controls (92.50 ± 13.72 cells / mm ~ 2; P = 0.03) 7.3 cells / mm ~ 2) was signif The numbers of RGCs in groups 2,3 (57.3 ± 8.2 cells / mm ~ 2,60.5 ± 12.9 cells / mm ~ 2) were comparable with those of group 5 (P = 0.18 and P = 0.31). The apoptosis rates with TUNEL staining also also parallel to RGC number. Animally with experimentally induced glaucoma showed an increase in retinal GFAP immunoreactivity. · CONCLUSION: Decrease in RGC loss and apoptosis suggest the neuroprotective potential of oral rosuvastatin treatment in a rat model of ocular hypertension. Host intravitreal rosuvastatin showed a contrary effect and further studies are required.