黄芪甲苷对糖尿病性白内障 SD 大鼠晶状体组织的MDA、SOD 及 GSH-Px 水平的影响研究

目的 探讨黄芪甲苷对糖尿病性白内障大鼠晶状体组织氧化应激损伤的保护作用。 方法 将 120 只 SD 大鼠随机选取 30 只作为对照组,剩余 90 只大鼠腹腔注射 55 mg / kg 链脲佐菌素( STZ)溶液建立糖尿病模型。 建模成功后,随机分为模型 组、低 剂 量 干 预 组 及 高 剂 量 干 预 组,每 组 30 只。 低 剂 量 干 预 组 和 高 剂 量 干 预 组 分 别 给 予120 mg / kg 和 240 mg / kg 黄芪甲苷,连续灌胃 12 周。 分别于第 18 周和第 24 周对大鼠进行晶状体透明度检测,并于第 24 周结束 后,取 大 鼠 的 晶 状 体 组 织,检 测 晶 状 体 组 织 中 丙 二 醛 ( malondialdehyde, MDA ) 、 超 氧 化 物 歧 化 酶( superoxide dismutase, SOD)和谷胱甘肽过氧化物酶( glutathione peroxidase, GSH-Px) 的水平。 结果 第 18 周和第24 周,检测发现糖尿病模型组较对照组晶状体混浊程度明显加重( P<0. 05) ,干预组大鼠晶状体混浊程度明显低于糖尿病性白内障模型组大鼠( P<0. 05) ,高剂量干预组大鼠晶状体混浊程度明显低于低剂量干预组大鼠( P< 0. 05) 。第 24 周结束后,检测发现已经形成白内障的模型组大鼠晶状体 MDA 含量较正常对照组大鼠明显升高( P< 0. 05) ,晶状体 SOD 及 GSH-Px 含量较对照组明显降低( P<0. 05) ;两干预组较模型组大鼠晶状体 MDA 含量显著降低( P<0. 05) ,SOD 及 GSH-Px 含量显著增加( P < 0. 05) ;高剂量干预组较低剂量干预组大鼠晶状体 MDA 含量显著降低(P<0. 05) ,SOD 及 GSH-Px 含量显著增加( P<0. 05) 。 结论 黄芪甲苷能增强糖尿病性白内障大鼠晶状体组织中SOD 及 GSH-Px 活性,清除晶状体组织中的氧自由基,抑制脂质过氧化反应,降低 MDA 水平,并且对于预防糖尿病性白内障大鼠晶状体混浊也具有一定的作用,且高剂量的黄芪甲苷较低剂量的黄芪甲苷作用更加明显。

Effect of Astragaloside IV on MDA,SOD and GSH-Px Levels in Lens Tissue of SD Rats with Diabetic Cataract

Abstract: Objective To explore the protective effect of astragaloside IV on oxidative stress injury of lens tissue in diabetic cataract rats. Method Thirty SD rats were randomly selected from 120 rats as the control group, and the remaining 90 rats were intraperitoneally injected with 55 mg / kg streptozotocin ( STZ ) solution to establish the diabetes models. After successful modeling, it was randomly divided into the diabetic model group, the low-dose intervention group and the high-dose intervention group. Each group was 30 rats. The low-dose and high-dose groups were given 120 mg / kg and 240 mg / kg of astragaloside IV for 12 weeks, respectively. The lens transparency was measured in the 3 groups of rats at the 18th and 24th weeks of the experiment. After the end of the 24th week, the lens tissues of the 4 groups of rats were taken to detect the levels of MDA, SOD and GSH-Px in the lens tissues. Result At the 18th and 24th weeks of the experiment, the lens transparency of the 4 groups of rats was found to be significantly increased in the diabetic model group compared with the control group ( P < 0. 05) . The lens opacity of the 2 groups was significantly lower than that of the diabetic model group. Rats in the model group ( P<0. 05) , the degree of lens opacity in the high-dose intervention group was significantly lower than that in the low-dose intervention group ( P<0. 05) . At the end of the 24th week, the contents of MDA, SOD and GSH-Px inthe lens tissues of the 4 groups were detected. The content of MDA in the lens of the model group with cataract formation was significantly higher than that in the control group ( P < 0. 05) , the contents of SOD and GSH-Px in the lens was significantly lower than that in the control group ( P<0. 05) . The content of MDA in the lens of the 2 groups was significantly lower than that in the model group ( P<0. 05) , and the contents of SOD and GSH-Px were significant. The increase of MDA content in the low-dose intervention group was significantly lower ( P<0. 05) , and the SOD and GSH-Px levels were significantly increased ( P < 0. 05) . Conclusion Astragaloside IV can enhance SOD and GSH-Px activities in lens tissue of diabetic cataract rats, clear oxygen free radicals in lens tissue, inhibit lipid peroxidation and reduce MDA levels. It also has a certain effect on preventing lens opacity in diabetic cataract rats. The higher dose of astragaloside IV is more effective in the lower dose of astragaloside.