Current eye research · 2012
A new and reliable animal model for optic nerve injury.
СтатьяНазвание и аннотация: Перевод в очереди
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Yan Hua, Li Fengling, Zhang Linlin
Аннотация
OBJECTIVE: To create an animal (rat) model of force percussion injury (FPI) to the optic nerve for clinical and experimental research.
METHODS: Seventy-one healthy female Wister rats, with no ocular disorders, were used in this study. Sixty-six rats were subjected to bilateral blunt trauma to the eyes via FPI; five rats were not subjected to trauma. According to the degree of optic nerve injury, injured eyes were divided into two groups: severe optic nerve injury group, with beat pressures of 699.14 ± 60.79 kPa and mild optic nerve injury group, with beat pressures of 243.18 ± 20.26 kPa. Eight rats were examined using flash visual-evoked potential (F-VEP) monitoring and magnetic resonance imaging (MRI) before, 1 and 3 days, and 1, 2, 4, 6, and 8 weeks after optic nerve injury. Fifty-six rats were examined by histopathology and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay for apoptosis at 1 and 3 days, and 1, 2, 4, 6, and 8 weeks after optic nerve injury. Two rats were examined by transmission electron microscopy (TEM) 4 and 8 weeks after optic nerve injury. The presence or absence of optic nerve injury was evaluated in all trauma eyes.
RESULTS: Latency was prolonged in the severe injury group compared with controls 1 day after optic nerve injury (p < .05). Amplitude decreased during the first 2 weeks after optic nerve injury (p < .05) and then stabilized (p > .05). Latency was prolonged in the mild optic nerve injury group compared with controls 1 day after optic nerve injury (p < .05) Amplitude decreased during the first 4 weeks (p < .05) following injury and then stabilized (p > .05). As measured by MRI, an abnormally high signal was seen 1 day after injury and remained significantly high 8 weeks after injury. A ruptured capillary was detected in the ganglion cell layer (GCL) 1 day after injury. Acellular regions in the ganglion cell layer were observed 4 weeks after optic nerve injury. TUNEL-positive cells were present in each layer of the retina 3 days after injury. The number of TUNEL-positive cells began to increase 1-2 weeks after injury, and then gradually decreased 4 weeks after injury (p < .05).
CONCLUSION: We successfully created a reproducible experimental animal (rat) model of optic nerve injury using FPI. Optic nerve injury was demonstrated by F-VEP and MRI, and confirmed histologically. Our model is a simple, reliable, reproducible, and stable tool for use in investigations on the mechanism(s) of and treatment for optic nerve injury.
METHODS: Seventy-one healthy female Wister rats, with no ocular disorders, were used in this study. Sixty-six rats were subjected to bilateral blunt trauma to the eyes via FPI; five rats were not subjected to trauma. According to the degree of optic nerve injury, injured eyes were divided into two groups: severe optic nerve injury group, with beat pressures of 699.14 ± 60.79 kPa and mild optic nerve injury group, with beat pressures of 243.18 ± 20.26 kPa. Eight rats were examined using flash visual-evoked potential (F-VEP) monitoring and magnetic resonance imaging (MRI) before, 1 and 3 days, and 1, 2, 4, 6, and 8 weeks after optic nerve injury. Fifty-six rats were examined by histopathology and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay for apoptosis at 1 and 3 days, and 1, 2, 4, 6, and 8 weeks after optic nerve injury. Two rats were examined by transmission electron microscopy (TEM) 4 and 8 weeks after optic nerve injury. The presence or absence of optic nerve injury was evaluated in all trauma eyes.
RESULTS: Latency was prolonged in the severe injury group compared with controls 1 day after optic nerve injury (p < .05). Amplitude decreased during the first 2 weeks after optic nerve injury (p < .05) and then stabilized (p > .05). Latency was prolonged in the mild optic nerve injury group compared with controls 1 day after optic nerve injury (p < .05) Amplitude decreased during the first 4 weeks (p < .05) following injury and then stabilized (p > .05). As measured by MRI, an abnormally high signal was seen 1 day after injury and remained significantly high 8 weeks after injury. A ruptured capillary was detected in the ganglion cell layer (GCL) 1 day after injury. Acellular regions in the ganglion cell layer were observed 4 weeks after optic nerve injury. TUNEL-positive cells were present in each layer of the retina 3 days after injury. The number of TUNEL-positive cells began to increase 1-2 weeks after injury, and then gradually decreased 4 weeks after injury (p < .05).
CONCLUSION: We successfully created a reproducible experimental animal (rat) model of optic nerve injury using FPI. Optic nerve injury was demonstrated by F-VEP and MRI, and confirmed histologically. Our model is a simple, reliable, reproducible, and stable tool for use in investigations on the mechanism(s) of and treatment for optic nerve injury.