摘要
目的:建立大鼠糖尿病性白内障模型,并探讨糖尿病大鼠晶状体混浊可能的发生机制.方法:采用一次性腹腔内注射链脲佐菌素(STZ)(65 mg/kg)的方法建立大鼠糖尿病模型.每周监测大鼠血糖、尿糖、体重的变化,并在裂隙灯下观察大鼠晶状体混浊的进展.第13周测定晶状体中谷胱甘肽还原酶(GR)、过氧化氢酶(CAT)活力以及谷胱甘肽(GSH)、糖化蛋白的含量.结果:70%(14/20)达成模标准,并出现糖尿病表现,其中1只大鼠(1/14)因血糖恢复至正常水平而被剔除.糖尿病大鼠晶状体混浊呈两阶段发展,前8wk缓慢进展及后5 wk快速进展.糖尿病组与正常对照组晶状体中CAT(nkat,479.3±339.0vs1002.0±467.6),GSH(mg/g,55.2±32.6vs102.7±39.1),糖基化蛋白(每摩尔蛋白中生成糖基化蛋白的毫摩尔数,5.4±0.5vs4.17±0.4)比较,有统计学差异(P<0.05).结论:一次性腹腔内注射STZ致大鼠糖尿病模型是研究糖尿病性白内障的可靠模型,晶状体蛋白糖基化反应及氧化损伤可能在糖尿病性白内障发生起重要作用.
AIM： To set up the diabetic cataract model and to explore the mechanism of diabetic cataract in rats induced by streptozotocin （STZ）. METHODS： Diabetic rats were made by a single intaperitoneal injection of STZ （65 mg/kg）. The changes of plasma glucose, urine glucose and body weight were monitored and the progression of lens opacification was recorded using the slit lamp every week. At 13th week, the levels of glutathione reductase （GR）, catalase （CAT）, glutathione （GSH） and glycated protein in lens were determined. RESULTS： About 70% （14/20） of the rats responded to the streptozotocin injection and the diabetic symptoms were observed in these rats. Only one rats （1/14） was rejected for the decrease of plasma glucose （ 〈 14 mmol/L）. Lens opacification progressed in a biphasic manner in the diabetic rats, an initial slow progression during the first 8 weeks of diabetes followed by a steep increased lens opacification in the next 5 weeks. There was statistically significant difference between the diabetic group and the normal group in the level of CAT （nkat, 479.3 ±339.0 vs 1002.0 ±467.6）, GSH （mg/g, 55.2 ± 32.6 vs 102.7 ± 39.1 ） and glycated protein （ mmol glycationpermolprotein, 5.4 ±0.5 vs4.17 ±0.4） （P〈0.05）. CONCLUSION：The diabetic model induced by a single intaperitoneal injection of streptozotocin was reliable for study in diabetic cataract. Lens protein glycation and oxidative damage may play some significantcant roles in the development of diabetic cataract.
出处
《第四军医大学学报》
北大核心
2006年第13期1208-1210,共3页
Journal of the Fourth Military Medical University
基金
国际合作研究项目基金(International Development Research Award
No:070667/Z/03)
