摘要：AIM:To study the effect of Ketangte2 (KTT2)on reducing blood glucose and its mechanism.METHODS:Adrenalin and streptozocin were used to induce hyperglycemia in two mice models,and then treated them with glybenzcyclamide (50 mg/kg),three different dose of KTT2 and normal saline(NS)(0.1 ml/10 g weight)for 15 days.And other healthy mice were set up as control group,During the experiment,the fast blood glucose(FBG),insulin was measured in different time.The pancreas and islets of diabetic mice induced by STZ were studied by pathologic section.RESULTS:In the adrenalin-induced model group,KIT2 could lighten hyperglycemic reaction,which Was significant different from that of model group(P＜0.05 or 0.01),while KTT2 high,middle dose group could decrease blood glucose in streptozocin-induced hypoglycemic mice obviously(P＜0.01).Histological examination showed that pancreatic island number in pancreas in KTT2 groups increased in comparison with the model group.CONCLUSION:KTT2 can obviously reduce the blood glucose in the two kinds of animal models of hyperglycemia (P＜0.05 or 0.01).Its mechanism may be related to the protective effect on islet β cells,thereby increase the insulin secretion.%目的:研究克糖特2号的降血糖作用及其作用机理.方法:采用肾上腺素和链脲霉素分别建立高血糖小鼠模型,分别用格列本脲(50 mg/kg)、3种不同剂量的克糖特2号和等体积生理盐水(0.1 mL/10 g体重)灌胃15 d,并另取健康小鼠作正常对照.并在相应时间采血测定糖尿病小鼠模型空腹血№糖(FBG)、胰岛素水平,同时对STZ所致糖尿病小鼠进行胰腺病理切片检查.结果:在肾上腺素诱发的高血糖症小鼠中,克糖特2号能够减轻高血糖反应,与模型组比较,有显著性差异(P＜0.05或0.01);克糖特2号高、中剂量组能明显降低链脲霉素致高血糖小鼠的血糖(P＜0.01).组织学研究可见克糖特2号组小鼠胰腺组织中的胰岛数目较模型组增多.结论:克糖特2号能显著降低2种高血糖动物模型的血糖水平(P＜0.05或0.01).其作用机制可能与修复、改善受损的胰岛细胞功能,促进胰岛素分泌有关.
