XGY对糖尿病小鼠的降血糖作用及其机制研究

Study of the Effect of XGY on Experiment Diabetes and Its Mechanisms

目的观察XGY对糖尿病小鼠血糖的影响。方法采用链脲菌素（STZ）和肾上腺素（Adr）复制小鼠糖尿病模型，0．1、0．2、0．4g／kgXGY灌服，观察其给药不同时间的降血糖作用。结果（1）0．2、0．4g／kgXGY组灌服8d后血糖即明显降低，与模型组比较差异显著（P〈0．05）；15d后，0．1、0．2、0．4g／kgXGY组血糖降低更明显（P〈0．01）。在注射STZ后，STZ糖尿病小鼠血清胰岛素水平显著下降，与正常组比较差异显著（P〈0．01）；灌服XGY15d后，血清胰岛素有增加的趋势，XGY大剂量组能显著增加血清胰岛素水平（P〈0．01）。（2）0．2、0．4g／kgXGY组可明显对抗Adr升高血糖的作用（P〈0．05）。（3）0．1、0．2、0．4g／kgXGY组能降低正常小鼠口服糖负荷后血糖的峰值（P〈0．05～0．01），并加快已升高的血糖水平回落的速度；同时能显著增加动物肝糖元含量（P〈0．05～0．01）。结论XGY可对抗STZ和Adr引起的血糖升高，改善糖耐量，增加肝糖元合成；作用机制可能与其促进胰岛素分泌或增加组织对糖的转化利用有关。

Objective To study the effect of XGY on experimental diabetes and its mechanism. Methods 0.1,0.2, 0.4 g/kg was given by XGY ig at various time to observe its effects of reducting in serum glucose in mice with STZ-induced diabetic and adrenaline hyperglycemia. Results （1） XGY 0.1,0.2, 0.4 g/kg given by XGY ig could reduce serum glucose in mice with STZ-induced diabetic at the 8th and 15th day respectively （P （0.05-0.01）. XGY with 0.4 g/kg could increase serum insulin level in mice with STZ-induced diabetic after ig for 15 days. （2）XGY showed a significant antagonistic effect on the serum glucose increased by Adr （P （ 0.05 - 0.01）, 0.1, 0.2, 0.4 g/kg XGY significantly increased the liver glycogen and reduced serum glucose （ P （ 0.05 - 0.01 ）. （3） XGY with 0.2, 0,4 g/kg after glucose （2.5 g/kg） was given, reduced the peak value of blood glucose （P （0.05） and speeded up restoration of the increased serum glucose level. Conclusion XGY can significantly check the STZ and Adr-induced rise of serum glucose, improve glucose tolerance and increase hepatic glueogen synthesis. It suggests that this mechanism of reducing serum glucose is associated with XGY function of promoting regeneration of islet β cells or increasing tissue transformation and glucose utilization.