Neuroprotective effect of systemic and/or intravitrea rosuvastatin administration in rat glaucoma model
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...
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Published in | 国际眼科杂志:英文版 Vol. 9; no. 3; pp. 340 - 347 |
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Main Author | |
Format | Journal Article |
Language | English |
Published |
2016
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Online Access | Get full text |
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Summary: | 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 (lOP) elevation was seen (P=0.002). Elevated lOP resulted in a significant decrease in number of RGCs in group 5 (70.33 ±8.2 cells/mm2) when compared with controls (92.50 ±13.72 cells/mm2; P=0.03). The RGC number in group 1 (92.4±7.3 cells/mm2) was significantly higher than group 5 (ρ=0.03). The numbers of RGC in groups 2, 3 (57.3±8.2 cells/mm2, 60.5±12.9 cells/mm2) were comparable with that of group 5 (ρ=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 immunoreacUvity. CONCLUSION: Decrease in RGC loss and apoptosis suggest the neuroprotective potential of oral rosuvastatin treatment in a rat model of ocular hypertension. Howeverintravitreal rosuvastatin showed a contrary effect and further studies are required. |
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Bibliography: | 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 (lOP) elevation was seen (P=0.002). Elevated lOP resulted in a significant decrease in number of RGCs in group 5 (70.33 ±8.2 cells/mm2) when compared with controls (92.50 ±13.72 cells/mm2; P=0.03). The RGC number in group 1 (92.4±7.3 cells/mm2) was significantly higher than group 5 (ρ=0.03). The numbers of RGC in groups 2, 3 (57.3±8.2 cells/mm2, 60.5±12.9 cells/mm2) were comparable with that of group 5 (ρ=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 immunoreacUvity. CONCLUSION: Decrease in RGC loss and apoptosis suggest the neuroprotective potential of oral rosuvastatin treatment in a rat model of ocular hypertension. Howeverintravitreal rosuvastatin showed a contrary effect and further studies are required. KEYWORDS: rat glaucoma model; retinal ganglion cellnumber; rosuvastatin; neuroprotection |
ISSN: | 2222-3959 2227-4898 |