摘要
目的 探讨一氧化氮合酶(nitricoxidesynthase ,NOS)活性异常变化在视网膜光损伤发生机制中的作用。方法 60只SD大鼠随机分为5组,1组为正常对照,其它4组以持续强光照射6小时造成视网膜光损伤,并按光照后1天和6天两个观察点各分为实验组与空白对照组,实验组大鼠给予左旋硝基精氨酸治疗,并分别测定比较各组大鼠视网膜外核层厚度以及NOS和超氧化物歧化酶(superoxidedismutase ,SOD)的活性。结果 光损伤后第1天和第6天空白对照组大鼠视网膜内NOS的活性均异常升高,SOD活性均显著下降,视网膜外核层厚度进行性减小;实验组大鼠视网膜内NOS的活性低于正常水平,SOD活性和视网膜外核层厚度均显著高于相应的空白对照组。结论 过度光照后视网膜内NOS活性持续异常升高是视网膜氧化损伤的重要原因并与感光细胞退行性变性的发生密切相关。
Objective To investigate the effect of abnormal activity of nitric oxide synthase (NOS) in the pathogenesis of light_induced retina injury. Methods 60 SD rats were divided into 5 groups at random. One group was taken as normal control and light damage was induced in the other 4 groups by exposure to constant intense light for 6 hours. Then these 4 groups were divided into empty controls and experimental groups according to the different observing time points, 1 day or 6 days after light exposure. Rats in the experimental groups received therapy with L_NNA. The thickness of the outer nuclear layer (TONL) and the activity of NOS and superoxide dismutase (SOD) in retina were determined respectively. Results The activity of NOS in retina of the empty controls were found to increase continuously after light damage, while the activity of SOD and the TONL decreased obviously. In the experimental groups, the activity of NOS were inhibited below the normal level, while the activity of SOD and the TONL were found significantly higher than their corresponding empty controls respectively. Conclusion The continuous enhanced activity of NOS after overwhelming light exposure plays an important role in the oxidative injury of retina and has close relationship with the retrograde degeneration of photoreceptors.
出处
《眼外伤职业眼病杂志》
北大核心
2005年第4期246-248,共3页
Journal of Injuries and Occupational Diseases of the Eye with Ophthalmic Surgeries
关键词
视网膜
光损伤
一氧化氮合酶
retina
light injury
nitric oxide synthase
