摘要
AIM: To investigate the effect of aminoguanidine(AG) on the expression of caspase-3 in rat retina after ischemiareperfusion injury.METHODS: The rats were anesthetized with 30mg/kg sodium pentobarbital introperitoneal(ip) injections.After topical application of 10g/L dicaine,the anterior chamber was punctured with a 5-gauge needle connected to a bottle containing normal saline.Intraocular pressure was raised to 100 mmHg by elevating the saline container.The infusion needle was removed from the anterior chamber 60 minutes later.Reperfusion of the retinal vasculature was confirmed by fundus examination.AG 100mg/kg was ip injected in drug group.The rats were then euthanatized at 6,24,and 72 hours after reperfusion,and their eyes were enucleated for immunohistochemistry.RESULTS: No specific staining was detected by using the caspase-3 antibody in the retina of control group.In ischemia group,the protein of caspase-3 was over-expressed at 6 hours and relieved at 24 hours and 72 hours,while with drug treatment,the expression of protein of caspase-3 was decreased at each time point.CONCLUSION: AG provides retinal protection against ischemia-reperfusion injury in rat retina,probably through an inducible NOS-dependent mechanism.
AIM: To investigate the effect of aminoguanidine (AG) on the Expression of caspase-3 in rat retina after ischemia-reperfusion injury. METHODS: The rats were anesthetized with 30mg/kg sodium pentobarbital introperitoneal (ip) injections. After topical application of 10g/L dicaine, the anterior chamber was punctured with a 5-gauge needle connected to a bottle containing normal saline. Intraocular pressure was raised to 100 mmHg by elevating the saline container. The infusion needle was removed from the anterior chamber 60 minutes later. Reperfusion of the retinal vasculature was confirmed by fundus examination. AG 100mg/kg was ip injected in drug group. The rats were then euthanatized at 6, 24, and 72 hours after reperfusion, and their eyes were enucleated for immunohistochemistry. RESULTS: No specific staining was detected by using the caspase-3 antibody in the retina of control group. In ischemia group, the protein of caspase-3 was over-expressed at 6 hours and relieved at 24 hours and 72 hours, while with drug treatment, the expression of protein of caspase-3 was decreased at each time point. CONCLUSION: AG provides retinal protection against ischemia-reperfusion injury in rat retina, probably through an inducible NOS-dependent mechanism.
