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阿司匹林对半乳糖性白内障抑制作用的实验研究
引用本文:喻继兵,周辉. 阿司匹林对半乳糖性白内障抑制作用的实验研究[J]. 眼科研究, 2009, 27(11): 1015-1018
作者姓名:喻继兵  周辉
作者单位:宁波大学医学院附属医院眼科,315020
摘    要:目的观察阿司匹林对大鼠半乳糖性白内障的抑制作用。方法将60只Wistar大鼠分为3组:半乳糖组每日腹腔注射80%的D-半乳糖(20mL/kg),连续10d,制成白内障动物模型;阿司匹林组同半乳糖组处理的同时每日给予阿司匹林混悬液150mg/kg灌胃至实验结束;对照组无特殊处理。实验前及造模起第3、6、10、14、20天行裂隙灯显微镜观察晶状体情况并拍照;造模起第5天各组随机处死8只大鼠,右眼晶状体匀浆检测超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、过氧化氢酶(CAT)的活性,左侧晶状体行扫描电镜观察并定量分析。结果对照组晶状体始终透明,实验第3、6、10、14、20天阿司匹林组白内障的发生率分别为0、25%、41.67%、58.33%、83.33%,大多数为囊泡初期,而半乳糖组第3天白内障发生率达65%,第6天后晶状体均发生混浊,最终发展为成熟期白内障;实验第5天扫描电镜下见对照组组织结构正常,半乳糖组损伤严重,阿司匹林组损伤较轻微;与对照组比较,半乳糖组SOD、GSH-PX、CAT活性明显降低(P〈0.05),阿司匹林组各酶活性强于半乳糖组(P〈0.05)。结论阿司匹林能增强晶状体中SOD、GSH-PX、CAT的活性,对大鼠半乳糖性白内障有抗氧化作用,从而延缓早期白内障的发生发展。

关 键 词:阿司匹林  白内障  超氧化物歧化酶  谷胱甘肽过氧化物酶  过氧化氢酶  超微结构  氧化损伤

The prevention effect of aspirin on galactose cataract
Yu Jibing,Zhou Hui. The prevention effect of aspirin on galactose cataract[J]. Chinese Ophthalmic Research, 2009, 27(11): 1015-1018
Authors:Yu Jibing  Zhou Hui
Affiliation:( Department of Ophthalmology,Affiliated Hospital of Medical College of Ningbo University, Ningbo 315020, China)
Abstract:Objective Experimental research demonstrated that oxidative damage leads to formation of cataract in rats and its machanism is the decline of activities of superoxide dismutase(SOD), glutathione peroxidase(GSH-PX) and catalase(CAT) . Aaspirin can improve the antioxidative ability of lens. The purpose of this study was to observe the inhibition of aspirin on D-Galactose-induced cataractous lenses of rats. Methods Galactose cataract model was established in 40 cleaning Wistar rals by intraperitoneal injection of 20 mL/kg 80% D-Galactose for 10 days. The models were divided into model group (20 rats) and aspirin group(20 rats). 150 mg/kg of aspirin was administered immediately by gastrogavaging in aspirin group for 20 days. Other 20 normal Wistar rats were as control group. At day 3, 6, 10, 14, 20, the transparency of rat lenses was observed under the slit lamp microscopy. At day 5 after experiment, the ultrastructure of the lenses was examined and evaluated under the scanning electron microscopy. The activities of SOD, GSH-PX and CAT were detected by Coomassie Brilliant Blue color comparator, respectively. The use of experimental animal followed the Regulations for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission. Results All lenses were transparent in the rats of control group. The degree of lens opacity was more mild in asprin group compared with model group. 25. 00%, 41. 67%, 58. 33%, 83. 33% of lenses in aspirin group showed swelling at day 6, 10, 14, 20, respectively, but 65% lenses were opacity in model group on day 3 and 100% lenses were nuclear cataracts in 6 days. The structure of lenses was normal in control group, but the process number, fiber thickness and fiber density of lens were significantly increased in model group compared with control group (P <0. 05), and only process number was increased in asprin group. The activities of SOD, GSH-PX and CAT in lens of model group were obviously lower than in normal control group(P<0. 05), but those in asprin group were significantly increased in comparison with model group(P <0. 05). Conclusion Aspirin could protect lenses of rats against oxidative damage by elevating activities of SOD, GSH-PX and CAT in lens and inhibiting the generation and development of galactose-induced cataract at early stage of cataract.
Keywords:aspirin  cataract  superoxide dismutase  glutathione peroxidase  catalase  ultrastructure  oxygen damage
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