消旋-α-硫辛酸对大鼠糖尿病性白内障抑制作用的研究

Effects of DL-α-lipoic acid on the experimentally induced diabetic cataract in rats

目的 探讨消旋 α 硫辛酸 (LA)对大鼠糖尿病性白内障的抑制作用。方法 将 7周龄雌性Brown Norway(BN)无特定病原体大鼠随机分为正常组 (8只 )、异常组 (14只 )及治疗组 (14只 )。使用链脲霉素 (STZ)制作异常组和治疗组糖尿病模型 ,治疗组大鼠饲料中添加 0 .3%LA。观察 3组大鼠晶状体散乱光强度、血糖浓度及晶状体中谷胱甘肽的水平。结果 注射STZ后 2周末 ,异常组出现晶状体前囊膜下网状混浊 ,并随时间加重 ,逐渐扩大至晶状体前皮质 ;4周末 ,治疗组晶状体前囊膜下轻微混浊 ;5周末 ,治疗组晶状体散乱光强度与异常组比较 ,差异有非常显著意义 (P <0 .0 1)。注射STZ后 3d ,治疗组血糖浓度与异常组比较 ,差异无显著意义 (P >0 .0 5 ) ;注射STZ后 80d ,治疗组血糖浓度明显低于异常组 (P <0 .0 1)。注射STZ后 10个月治疗组晶状体中谷胱甘肽的浓度与异常组比较 ,差异无显著意义 (P >0 .0 5 )。结论 口服LA可有效降低STZ所致糖尿病大鼠的血糖浓度 ,抑制白内障发生。LA在晶状体中的生化特性尚待深入研究。

Objective To investigate whether DL-α-lipoic acid (LA) can offer lenticular protection in diabetic rats. Method 36 Brown-Norway (BN) specific pathogen free (SPF) rats (7 week-old, female), were divided into 3 groups comprising of the diabetes mellitus (DM)group (14 rats), the diabetes mellitus treated with LA (DM+LA) group (14 rats), and the control(CTL)group (8 rats). The diabetic cataract was induced by streptozotocin (STZ) injection. Powdered food mixed with 0.3%LA was given to the DM+LA group, 3 days after STZ injection. Lens density was measured with EAS-1000, blood glucose and lens glutathione concentration was examined. Result 2 weeks after STZ injection, there was a subcapsular reticular opacity in the DM; Lens opacity became more severe and enlarged with increased duration of STZ exposure. 4 weeks later, there was slight lens opacity in the DM+LA group. After 5 weeks, there were significant differences in lens densities between the DM and the DM+LA groups( P <0.01). 3 days after STZ injection, there was no difference between the DM and the DM+LA in blood glucose( P >0.05); At 80 days, the concentration of blood glucose in the DM+LA was less than that of in the DM ( P <0.01). 10 months after STZ injection, there was no difference of the concentration of glutathione in lens between the DM+LA and the DM ( P >0.05). Conclusion LA ingested orally can effectively reduce STZ-induced blood glucose and inhibit diabetic cataractogenesis in rats.