黄芩苷、二甲双胍和氨基胍对D-半乳糖诱导大鼠体内蛋白非酶糖基化-氧化应激、醛糖还原酶活性及胰岛素抵抗作用

目的：观察黄芩苷、二甲双胍和氨基胍对D-半乳糖诱导大鼠体内蛋白非酶糖基化-氧化应激、醛糖还原酶活性及胰岛素抵抗作用。方法：清洁级健康SD大鼠90只,完全随机分为6组正常对照组、模型对照组、氨基胍组、二甲双胍组、黄芩苷高剂量和黄芩苷低剂量组,每组各15只。除空白对照组外,其余组大鼠均采用腹腔注射D-gal,灌胃;结束时观察各组大鼠晚期糖基化终末产物、糖化血红蛋白、胰岛素等,并计算胰岛素敏感指数,醛糖还原酶和超氧化物歧化酶的活性。结果：D-gal处理大鼠出现血糖升高、糖耐量减退、糖基化产物及胰岛素含量增高,SOD活性降低及红细胞内AR活性增强;Met,AG以及Bai高和低剂量均能改善D-gal诱导大鼠IGT和降低糖基化产物和胰岛素含量。结论：D-gal诱导能使大鼠体内糖基化反应、胰岛素抵抗和醛糖还原酶活性增强;Bai,Met和AG能抑制蛋白非酶糖基化反应和醛糖还原酶活性,改善高胰岛素血症。

Effects of baicalin,metformin and aminoguanidine on D-galactose-induced non-enzymatic protein glycosylation-oxidative stress,aldose reductase activity and insulin resistance in rats

Objective：To observe the effects of baicalin （ Bai ） , metformin （ Met ） and aminoguanidine （ AG ） on D-galactose （ D-gal ）-induced non-enzymatic protein glycation-oxidative stress, aldose reductase activity,and insulin resistance in rats.Method：90 clean and healthy SD rats were randomly divided into normal control group,model control group,aminoguanidine group,high-dose baicalin group and low-dose baicalin group, with 15 rats in each group. Except for the normal control group, the rats in other groups were intraperitoneally injected with D-gal and given gavage;in the end of the experiment,advanced glycation end-products,glycosylated hemoglobin,and insulin in each group were observed,insulin sensitivity index was calculated,and the activity of aldose reductase as well as superoxide dismutase were determined.Results：The rats given D-gal had raised blood glucose,decreased sugar tolerance,increased contents of glycosylation products and insulin,reduced SOD activity, and enhanced AR activity in red blood cells. Met, AG and high-and-low dose Bai could improve IGT in D-gal induced rats and reduce the contents of glycosylation products and insulin. Conclusions：D-gal can induce enhanced glycosylation reaction, insulin resistance, and aldose reductase activity in rats. Bai, Met and AG can inhibit non-enzymatic protein glycation and aldose reductase activity,and improve hyperinsulinemia.