眼科研究
眼科研究
안과연구
CHINESE OPHTHALMIC RESEARCH
2009年
11期
1015-1018
,共4页
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
阿司匹林%白內障%超氧化物歧化酶%穀胱甘肽過氧化物酶%過氧化氫酶%超微結構%氧化損傷
아사필림%백내장%초양화물기화매%곡광감태과양화물매%과양화경매%초미결구%양화손상
aspirin%cataract%superoxide dismutase%glutathione peroxidase%catalase%ultrastructure%oxygen damage
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.
目的 觀察阿司匹林對大鼠半乳糖性白內障的抑製作用.方法 將60隻Wistar大鼠分為3組:半乳糖組每日腹腔註射80%的D-半乳糖(20mL/kg),連續10d,製成白內障動物模型;阿司匹林組同半乳糖組處理的同時每日給予阿司匹林混懸液150mg/kg灌胃至實驗結束;對照組無特殊處理.實驗前及造模起第3、6、10、14、20天行裂隙燈顯微鏡觀察晶狀體情況併拍照;造模起第5天各組隨機處死8隻大鼠,右眼晶狀體勻漿檢測超氧化物歧化酶(SOD)、穀胱甘肽過氧化物酶(GSH-PX)、過氧化氫酶(CAT)的活性,左側晶狀體行掃描電鏡觀察併定量分析.結果 對照組晶狀體始終透明,實驗第3、6、10、14、20天阿司匹林組白內障的髮生率分彆為0、25%、41.67%、58.33%、83.33%,大多數為囊泡初期,而半乳糖組第3天白內障髮生率達65%,第6天後晶狀體均髮生混濁,最終髮展為成熟期白內障;實驗第5天掃描電鏡下見對照組組織結構正常,半乳糖組損傷嚴重,阿司匹林組損傷較輕微;與對照組比較,半乳糖組SOD、GSH-PX、CAT活性明顯降低(P＜0.05),阿司匹林組各酶活性彊于半乳糖組(P＜0.05).結論 阿司匹林能增彊晶狀體中SOD、GSH-PX、CAT的活性,對大鼠半乳糖性白內障有抗氧化作用,從而延緩早期白內障的髮生髮展.
목적 관찰아사필림대대서반유당성백내장적억제작용.방법 장60지Wistar대서분위3조:반유당조매일복강주사80%적D-반유당(20mL/kg),련속10d,제성백내장동물모형;아사필림조동반유당조처리적동시매일급여아사필림혼현액150mg/kg관위지실험결속;대조조무특수처리.실험전급조모기제3、6、10、14、20천행렬극등현미경관찰정상체정황병박조;조모기제5천각조수궤처사8지대서,우안정상체균장검측초양화물기화매(SOD)、곡광감태과양화물매(GSH-PX)、과양화경매(CAT)적활성,좌측정상체행소묘전경관찰병정량분석.결과 대조조정상체시종투명,실험제3、6、10、14、20천아사필림조백내장적발생솔분별위0、25%、41.67%、58.33%、83.33%,대다수위낭포초기,이반유당조제3천백내장발생솔체65%,제6천후정상체균발생혼탁,최종발전위성숙기백내장;실험제5천소묘전경하견대조조조직결구정상,반유당조손상엄중,아사필림조손상교경미;여대조조비교,반유당조SOD、GSH-PX、CAT활성명현강저(P＜0.05),아사필림조각매활성강우반유당조(P＜0.05).결론 아사필림능증강정상체중SOD、GSH-PX、CAT적활성,대대서반유당성백내장유항양화작용,종이연완조기백내장적발생발전.
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.
