氨基胍滴眼液防治大鼠糖尿病性白内障的研究

Study on the prevention of diabetic cataracts by aminoguanidine eye-drops in rats

目的探讨氨基胍对链脲佐菌素诱导的大鼠糖尿病性白内障的防治效果及其作用机制。方法采用一次性腹腔内注射链脲佐菌素(65mg·kg-1)的方法建立大鼠糖尿病模型,血糖值大于14mmol·L-1为成模标准。治疗组左眼滴氨基胍溶液,2次·d-1。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活力、过氧化氢酶、谷胱甘肽以及糖化蛋白的含量。结果71%(32/45)达成模标准,并出现糖尿病表现。糖尿病大鼠晶状体混浊呈2阶段发展,前8周缓慢进展及后5周快速进展。氨基胍眼液治疗可延缓糖尿病性白内障发生,第4周出现统计学差异(P<0.05)。氨基胍治疗组晶状体中糖基化蛋白含量明显低于未治疗组(P<0.05),氨基胍治疗组晶状体中谷胱甘肽含量较未治疗组有提高。结论氨基胍滴眼液可抑制早期糖尿病性白内障的进展,其抗糖基化蛋白作用可能参与抑制糖尿病性白内障的形成。

Objective To explore the effect and the mechanism of aminoguanidine on streptozotocin（ STZ）-induced diabetic cataract. Methods Diabetic rats models were established by a single intraperitoneal injection of STZ,and those rats （〉14 mmol·L^ -1 plasma glucose） were assigned as diabetic rats. Rats in the treated group received aminoguanidine eye-drops to the left eye, twice daffy. 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 glycation in lens were determined. Results About 71% （32/45） of the rats responded to the streptozotocin injection （ random plasma glucose 〉 14 retool· L^- 1 ） and the diabetic symptom was observed in these rats. Lens opacification progressed in a biphasic maimer in the diabetic rats, an initial slow increase during the first 8 weeks of diabetes followed by a steep increase in the next 5 weeks. Amtnoguantdlne treatment delayed the progression of cataracts in diabetic rats and the delay was statistically significant on the 4th week of diabetes. The level of glycation in the amtnoguantdtne treated diabetic rats was significant lower than that in the untreated diabetic rats（P〈0.001）.An increase of GSH in lens was observed in the amtnoguantdtne treated diabetic rats when compared with the untreated diabetic rats. Conclusion Aminoguanidine eye-drops treatment can delay the progression of cataracts in the early state of diabetic rats. Its anti-glycatton effect may contribute to the inhibition of the diabetic cataract formation.