摘要
目的:研究克糖特(KTF)对糖尿病模型小鼠血糖的影响,并初步探讨其降低小鼠血糖的作用机制。方法:建立链脲霉素(STZ)致糖尿病小鼠模型。将小鼠随机分为5组(n=10),分别用格列本脲(50 mg·kg^(-1))、高、中、低剂量克糖特和0.9%氯化钠溶液(0.1 ml/10g体重)灌胃15d。15d后测定正常小鼠的血糖水平,并在相应时间测定STZ致糖尿病小鼠模型空腹血糖(FBG)、药后2h血糖(2h BG)、胰岛素水平,同时对STZ所致糖尿病小鼠进行胰腺病理组织学检查。结果:克糖特对正常小鼠血糖水平无影响,能够显著降低STZ模型小鼠空腹血糖(与模型组比较降糖率可达24.39%,P<0.05～0.01)和药后2 h BG(P<0.05),明显提高胰岛素水平(P<0.05～0.01),保护胰岛β细胞。结论:克糖特对STZ引起的高血糖有较好的降糖作用,其作用机制可能与改善受损的胰岛细胞功能,促进胰岛素分泌有关。
To study the effects and its mechanism of Ketangte （KTT） on the blood sugar level in diabetic mice. Method： Diabetic mice were induced by intraperitoneal injection of streptozotocin （STZ） and then were divided into 5 groups, the mice were treated （ i. g. ） with glybenzcyclamide （ 50mg·kg^-1） , three different doses of KTT and normal saline （NS） respectively for 15 days. The levels of FBG, 2 hBC were measured in mice with experimental hyperglycemias induced by STZ after 15 days treatment of drugs. Insulin levels in diabetic mice induced by STZ were measured before and after the treatment of drugs, and the histopathological changes of pancreare was observed by light microscope. Result： KTT was able to reduce significantly the blood sugar level in STZ-induced diabetic mice, the blood sugar level was decreased by 24.39% compared with the model group（ P〈0.05 or 0.01 ）. But it had no effect on blood sugar level in normal mice. In addition, KTT could increase serum insulin level （ P〈 0.05 or 0.01 ） and have obvious protective effect on islet β-cells. Conclusion ： KTT can significantly reduce the blood sugar with dose dependent fashion in STZ-induced dia betic mice, and its mechanism may be related to the protective effect on islet β cells, resulting in the increased insulin secretion.
出处
《中国药师》
CAS
2007年第9期843-845,共3页
China Pharmacist
基金
广西自然科学基金项目(桂科自0447039)
