论文部分内容阅读
目的:探讨白簕中性均一多糖组分(ATP1-1)对链脲佐菌素(STZ)诱导的I型糖尿病小鼠的降糖作用及机制。方法:采用多次小剂量注射链脲佐菌素(MLD-STZ)的方法,建立C57BL/6小鼠I型糖尿病模型。成模小鼠随机分成高血糖模型组、二甲双胍组、ATP1-1高剂量组和ATP1-1低剂量组,以同周龄正常小鼠为正常对照组,每组10只,给药4周。于给药后检测小鼠空腹血糖值(FBG)以及肝糖原含量,采用RT-PCR的方法测定肝脏中葡萄糖激酶(GK)、葡萄糖6磷酸酶(G6Pase)、葡萄糖转运体2(GLUT2)mRNA表达水平。结果:与模型组相比,ATP1-1高、低剂量组的血糖均显著下降(p<0.05),其中40 mg·kg~(-1)ATP1-1给药组血糖抑制率为29.4%;两剂量组均可有效增加糖尿病小鼠肝糖原含量(p<0.05);RT-PCR结果显示,ATP1-1高、低剂量组GK mRNA、GLUT2 mRNA表达显著增加(p<0.01),G6Pase mRNA表达降低(p<0.05)。结论:ATP1-1可以有效降低糖尿病小鼠血糖,该作用机制与调节糖代谢中的关键酶及相关转运体有关。
Aims: To investigate the hypoglycemic effect and mechanism of neutral homo-polysaccharide (ATP1-1) in streptozotocin (STZ) -induced type 1 diabetic mice. Methods: C57BL / 6 mouse model of type 1 diabetes mellitus was established by multiple low-dose streptozotocin (MLD-STZ) injection. The model mice were randomly divided into hyperglycemia model group, metformin group, ATP1-1 high dose group and ATP1-1 low dose group. The normal mice of the same age were used as the normal control group, with 10 rats in each group for 4 weeks. The fasting blood glucose (FBG) and hepatic glycogen contents of the mice were measured after administration, and the levels of hepatic glucokinase (GK), glucose 6 phosphatase (G6Pase) and glucose transporter 2 (GLUT2) mRNA were determined by RT- The expression level. Results: Compared with the model group, the blood glucose of ATP1-1 high and low dose groups were significantly decreased (p <0.05), of which the plasma glucose inhibition rate was 29.4% in 40 mg · kg -1 ATP1-1 group. (P <0.05). The results of RT-PCR showed that the expression of GK mRNA and GLUT2 mRNA in high and low dose groups of ATP1-1 increased significantly (p <0.01), while the expression of G6Pase mRNA Decreased expression (p <0.05). Conclusion: ATP1-1 can effectively reduce the blood sugar in diabetic mice. The mechanism is related to the regulation of key enzymes and related transporters in glucose metabolism.