明月草总黄酮对2型糖尿病模型小鼠降血糖作用研究

目的 分析明月草总黄酮对2型糖尿病模型小鼠降血糖的作用。方法 采用腹腔灌注链尿佐菌素(STZ)配合高脂饲料复制2型糖尿病小鼠模型,并将其分成对照组、模型组、阳性组以及明月草总黄酮低、中、高剂量组。考察明月草总黄酮多模型小鼠体质量、空腹血糖、糖耐量及血清总胆固醇(TC)、血清甘油三脂(TG)及游离脂肪酸(NEFA)等血脂指标的影响。结果 给药2和4 周,明月草总黄酮中、高剂量组小鼠体质量、空腹血糖改善情况均优于低剂量组,且与低剂量组比较差异有统计学意义,中、高剂量组之间比较差异无统计学意义。各组血糖均于葡萄糖溶液灌胃后0.5 h达峰值,之后逐渐下降。灌胃后1.0 h,除对照组血糖外,其余各组血糖下降幅度大小顺序依次是:阳性组>高剂量组>中剂量组>低剂量组>模型组。给药4周时,明月草总黄酮低、中、高剂量组TC、TG及NEFA比较差异无统计学意义,但均低于模型组。结论 明月草总黄酮可较好地改善2型糖尿病模型小鼠空腹血糖及脂质代谢异常。

Hypoglycemic effect of total flavones of Angelica Keiskei on type 2 diabetic mice

Objective To analyze the hypoglycemic effect of total flavonoids from the leaves of Angelica Keiskei on type 2 diabetic mice.Methods The model of type 2 diabetic mice was maded by intraperitoneal perfusion streptozotocin (STZ) and high fat diet.The mice were divided into the control group,the model group,the positive group and the low,medium and high dose group of the total flavonoids of Angelica Keiskei.The effects of the body weight,fasting blood glucose,glucose tolerance,serum total cholesterol (TC),serum glycerin three fat (TG) and free fatty acid (NEFA) were investigated.Results When the drug was given 2 and 4 weeks, the improvement of body weight and fasting blood glucose in medium and high dose groups of the total flavonoids were better than those in the low dose group,and the difference was statistically significant,while there was no significant difference between the middle and high dose groups. The blood glucose of each group reached peak value at 0.5 h after the gavage, and then gradually decreased. 1 h after gavage, in addition to the control group, the order of decrease of blood glucose in other groups was as follow:Positive group＞high dose group>middle dose group＞low dose group>model group.When the drug was given 4 weeks,there was no significant difference in TC,TG and NEFA in the low,middle and high dose group of total flavonoids of Angelica Keiskei,but all were lower than that of the model group.Conclusion The total flavonoids of Angelica Keiskei could improve the fasting blood glucose and abnormal lipid metabolism in type 2 diabetic mice.