论文部分内容阅读
目的 观察实验兔眼球钝挫伤后不同时间视网膜抗氧化酶类及脂质过氧化水平的变化。方法 以重物下落法制成兔眼球钝挫伤模型 (轻型 ) ,并采用生化方法于伤前及伤后不同时点测定视网膜组织中脂质过氧化产物(MDA)的含量 ,超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH PX)及过氧化氢酶 (CAT)的活性。结果 MDA于伤后 1天时明显升高 ,3天时略有下降但仍高于正常 ,7天时回到正常水平。SOD活性于伤后 1天时低于正常 ,其后上升 ,3天时高于正常 ,以后再下降至 7天时达正常水平。GSH PX活性 1天时高于正常水平 ,其后下降 ,3天时仍低于正常 ,而至 7天时回到正常水平。CAT活性于伤后 1天时降低 ,以后逐渐回升 ,至 7天时回到正常水平。结论 自由基介导的脂质过氧化反应加剧是钝挫伤后视网膜损害的重要原因。挫伤后视网膜抗氧化酶类的变化 ,可能是机体清除自由基损害的防御性反应
Objective To observe the changes of retinal antioxidant enzymes and lipid peroxidation in experimental rabbits with blunt trauma at different time points. Methods Rabbit eye contusion blunt model (light) was made by heavy drop method. The content of lipid peroxidation product (MDA) in retinal tissue was measured by biochemical methods at different time points before and after injury. The content of superoxide dismutase SOD, GSH PX and CAT. Results MDA increased significantly 1 day after injury, slightly decreased at 3 days but still higher than normal, returned to normal level at 7 days. The activity of SOD was lower than normal at 1 day after injury, then increased, then higher than normal at 3 days, then dropped to normal level at 7 days later. GSH PX activity was higher than normal on day 1 and then decreased, still below normal on day 3, and back to normal on day 7. CAT activity decreased 1 day after injury, then gradually rose to 7 days to return to normal levels. Conclusions Radical-mediated lipid peroxidation aggravation is a major cause of retinal damage after blunt trauma. Changes in retinal antioxidant enzymes after contusion may be the body’s defensive response to free radical damage