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目的:观察虫草多糖对2型糖尿病小鼠InsR/IRS-1通路及糖代谢的影响。方法:采用高脂饲料联合腹腔注射小剂量链脲佐菌素(STZ,25 mg·k~(-1))建立胰岛素抵抗2型糖尿病模型,每日给予不同剂量虫草多糖(200,400 mg·kg~(-1))治疗,28 d后,免疫印迹法检测实验小鼠骨骼肌内胰岛素受体(InsR)、胰岛素受体底物(IRS-1)及葡萄糖转运蛋白(GLUT4)的表达水平。检测肝脏葡萄糖激酶(GK)、磷酸果糖激酶(PFK)活性水平。结果:虫草多糖治疗组可显著改善糖尿病小鼠InsR/IRS-1及GLUT4蛋白的异常表达(P<0.05);并呈剂量依赖性地增强小鼠肝脏GK及PFK酶活性,与糖尿病模型组比较差异有统计学意义(P<0.05或0.01)。结论:虫草多糖可增强胰岛素信号通路敏感性,改善葡萄糖代谢,从而缓解糖尿病小鼠胰岛素抵抗及高血糖症状,为胰岛素抵抗2型糖尿病的临床治疗提供新的依据。
Objective: To observe the effect of Cordyceps polysaccharide on InsR / IRS-1 pathway and glucose metabolism in type 2 diabetic mice. Methods: A model of insulin resistance type 2 diabetes mellitus was established by intraperitoneal injection of high fat diet and low dose streptozotocin (STZ, 25 mg · k ~ (-1)). Different doses of Cordyceps polysaccharide (200, 400 mg · kg ~ (-1)). After 28 days, the expression of insulin receptor (InsR), insulin receptor substrate (IRS-1) and glucose transporter (GLUT4) in skeletal muscle of experimental mice were detected by Western blotting. The levels of hepatic glucokinase (GK) and phosphofructokinase (PFK) activity were measured. Results: Cordyceps polysaccharide treatment group could significantly improve the abnormal expression of InsR / IRS-1 and GLUT4 protein in diabetic mice (P <0.05), and in a dose-dependent manner to enhance the liver GK and PFK enzyme activity in mice compared with the diabetic model group The difference was statistically significant (P <0.05 or 0.01). CONCLUSION: Cordyceps polysaccharides enhance the sensitivity of insulin signaling pathway and improve glucose metabolism, thereby relieving insulin resistance and hyperglycemia in diabetic mice and providing new evidence for the clinical treatment of type 2 diabetes mellitus with insulin resistance.