阿司匹林滴眼液防治糖尿病性白内障

目的:探讨阿司匹林滴眼液抑制糖尿病性白内障的作用效果及作用机制.方法:复制链脲佐菌素(streptozocin, STZ)糖尿病大鼠模型,成模后(血糖＞14 mmol/L)将动物分为低浓度阿司匹林治疗组(0.5 g/L)、高浓度阿司匹林治疗组(1 g/L)和未治疗组.治疗组每日给予2次阿司匹林滴眼液治疗左眼,采用裂隙显微镜观察并记录晶状体混浊的程度,使用分光光度计测定晶状体中谷胱甘肽、糖基化终末产物(advanced glycation end product, AGE)的含量以及谷胱甘肽还原酶、过氧化氢酶的活性.结果:建立糖尿病大鼠模型后6至9 wk,与糖尿病大鼠相比,治疗组大鼠晶状体混浊程度降低0.5～1个级别,谷胱甘肽的含量升高20%,过氧化氢酶的活性增强260%,而AGE的含量降低28%,它们之间差异均具有统计学意义(P＜0.05).结论:阿司匹林可能通过抑制晶状体蛋白质糖基化和氧化损伤的综合作用,延缓早期的糖尿病大鼠晶状体混浊.

Preventive effect of aspirin eye-drops against diabetic cataract

AIM: To investigate the role and mechanism of aspirin (Asp) eye-drops in preventing diabetic cataract. METHODS: Diabetic cataract was induced by streptozocin (STZ). The diabetic rats (blood glucose>14 mmol/L) were randomly divided into 3 groups: lower concentration aspirin treatment group (0.5 g/L), higher concentration aspirin treatment group (1 g/L) and untreated group . The former two groups received Asp eye-drops to the left eye, twice daily. Progression of lens opacification was recorded using slit lamp at regular time intervals. The levels of advanced glycation end products (AGE), glutathione reductase (GR), catalase (CAT), and glutathione (GSH) were determined spectrometically. RESULTS: Asp treatment delayed the progression of cataracts in diabetic rats and the delay was statistically significant from the 6th to the 9th week of diabetes (about 0.5-1 grade, P<0.05 vs untreated diabetic rats). An increase in CAT(about 260%) and GSH(about 20%)was found in the lens of Asp treated diabetic rats (P<0.05 vs untreated diabetic rats). The level of glycated lens protein in the untreated diabetic rats was significant higher as compared with that in Asp treated diabetic rats (28%, P<0.05). CONCLUSION: Asp can delay the progression of lens opacification only during the earlier stages. The delay may associate with the protective effect of Asp against inactivation of antioxidation enzymes and the formation of AGEs.