目的 通过研究地黄寡糖对2型糖尿病大鼠肝脏糖代谢关键酶活性和基因表达的影响, 揭示地黄寡糖治疗糖尿病的机制。 方法 Wistar雌性大鼠以高脂饲料喂养2月后, 一次性ip链脲佐菌素(STZ)30mg/kg诱发大鼠2型糖尿病。7d后大鼠分为模型组、地黄寡糖低和高剂量(100、200mg/kg)组、二甲双胍阳性对照组, 每天ig给药1次, 连续4周, 另设对照组。 给药4周后处死大鼠, 取肝脏检测肝糖原的量及葡萄糖激酶(GK)和葡萄糖-6-脱氢酶(G-6-Pase)活性, 用RT-PCR技术检测GK和G-6-Pase基因表达。 结果 与模型组相比, 地黄寡糖能显著增加肝糖原的量(P<0.01), 增强GK活性(P<0.01)和基因表达(P<0.05), 减弱G-6-Pase活性(P<0.01)及其基因表达(P<0.05)。 结论 地黄寡糖可能通过改善糖尿病大鼠肝糖代谢关键酶活性及基因表达发挥治疗糖尿病作用。

Objective To investigate the pharmacological mechanism of Rehmannia glutinosa oligosaccharides (RGO) on the activity and gene expression of hepatic glycometabolic key enzymes in type 2 diabetic rats. Methods Female Wistar rats were ip injected with STZ (30mg/kg) after fed with high lipid food for two months, then rats were divided into model, RGO low-and high-dose (100 and 200mg/kg), and positive control groups. Rats were killed after they had been ig administered once daily for four weeks, the content of the hepatic glycogen, the activity of GK and G-6-Pase were detected. Meanwhile, the gene expression of GK and G-6-Pase were determined by RT-PCR. Results Comparing with model group, RGO could improve the content of the hepatic glycogen (P<0.01) significantly, increase the activity (P<0.01) and gene expression (P<0.05) of GK, and reduce the activity (P<0.01) and gene expression (P<0.05) of G-6-Pase. Conclusion RGO exerts its anti-diabetic pharmacological effect by ameliorating the activities and gene expressions of hepatic glycometabolic key enzymes.

国家自然科学基金资助项目(30772073;81173620)；甘肃省自然科学基金资助项目(3ZS051-A25-078)