论文部分内容阅读
目的探讨清化颗粒治疗2型糖尿病的可能作用机制。方法 24只db/db糖尿病小鼠随机分为模型对照组和清化颗粒低、中、高剂量组各6只,另设6只db/m小鼠为空白对照组。清化颗粒低、中、高剂量组分别给予清化颗粒3.77、7.54、15.08 g/(kg·d)灌胃,模型对照组给予生理盐水10 ml/(kg·d)灌胃,空白对照组不做其他处理。各组均连续观察4周。实验结束后检测各组小鼠空腹血糖、血清糖化血红蛋白(Hb A1c)含量及血清胰高血糖素样肽1(GLP-1)浓度,并检测小鼠回肠组织中葡萄糖转运因子2(GLUT2)mRNA和蛋白水平。结果与空白对照组比较,模型对照组小鼠空腹血糖和Hb A1c含量明显升高,血清GLP-1浓度及回肠组织中GLUT2 mRNA和蛋白表达均明显降低(P<0.01)。与模型对照组比较,清化颗粒低、中、高剂量组均能下调空腹血糖和Hb A1c含量,上调血清GLP-1浓度及回肠组织中GLUT2mRNA和蛋白表达,并且以清化颗粒高剂量组效果最好(P<0.05或P<0.01)。结论清化颗粒能降低db/db糖尿病小鼠空腹血糖和Hb A1c水平,促进GLP-1分泌,其作用机制可能与上调回肠组织中GLUT2的表达有关。
Objective To investigate the possible mechanism of Qinghua Granule in treating type 2 diabetes mellitus. Methods Twenty-four db / db diabetic mice were randomly divided into model control group and Qinghua Granule group, 6 rats in each group, and 6 mice in db / m group as blank control group. Qinghua Granule was given to rats in low, middle and high dosage groups respectively by intragastric administration of Qinghua Granule 3.77, 7.54 and 15.08 g / (kg · d) respectively. The model control group was given normal saline 10 ml / (kg · d) No other treatment. All groups were observed for 4 weeks continuously. After the experiment, fasting blood glucose, serum HbA1c and GLP-1 were detected in each group, and the mRNA expression of glucose transporter 2 (GLUT2) in mouse ileum And protein level. Results Compared with the blank control group, the levels of fasting blood glucose and Hb A1c in model control group were significantly increased, and the concentration of GLP-1 and the expression of GLUT2 mRNA and protein in ileum were significantly decreased (P <0.01). Compared with the model control group, Qinghua Granules low, medium and high dose groups were able to down-regulate fasting blood glucose and Hb A1c levels, raise serum GLP-1 concentration and GLUT2 mRNA and protein expression in ileum tissue, Best (P <0.05 or P <0.01). Conclusion Qinghua Granules can reduce fasting blood glucose and Hb A1c levels and promote the secretion of GLP-1 in db / db diabetic mice, and its mechanism may be related to the up-regulation of GLUT2 expression in ileum.