毛平车前降血糖调血脂作用的研究

Studies on the hypoglycemia and lipids regulating effects of Plantago depressa var. montata

目的:研究毛平车前醇提取物(PDM)降血糖调血脂作用及机制。方法:观察PDM对正常小鼠血糖的影响;对四氧嘧啶糖尿病小鼠糖耐量,血糖、糖化血清蛋白(GSP)、胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDLC)、低密度脂蛋白胆固醇(LDLC)、超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO)及胰岛损伤程度的影响;用H2O2诱导人脐带静脉内皮细胞株ECV304细胞氧化损伤,观察PDM对血管内皮细胞损伤的保护作用。结果:PDM对正常小鼠血糖无明显影响,可明显降低糖尿病小鼠的糖耐量,显著降低糖尿病小鼠血糖及血清中GSP,TC,TG,LDLC,MDA含量,明显回升HDLC/TC比值、SOD活性和NO含量,并减轻四氧嘧啶对胰岛细胞的损伤;能明显提高损伤后ECV304细胞的存活率,使细胞培养液中SOD活性上升,降低细胞内MDA含量。结论:毛平车前具有显著的降血糖调血脂作用,作用机制可能与提高机体抗氧化能力、减轻自由基对胰岛细胞的损伤有关。

Objective： To investigate the effects of Plantago depressa var. montata. Extract （PDM） on the metabohsrns of glucose and lipids in mice as well as the underlined mechanism. Method： Fasting sertum glucose （FSG） in nomal mice was detemined after oral administration of PDM. The effects of PDM on diabetic mice induced by alloxan were investigated by observing the changes of glucose roles, the contents of FSG, gtycosylated senan protein （GSP）, total cholesterol （TC）, trigtyceride（TG）, low density lipoprotein cholesterol （IDL-C）, high density lipoprotein cholesterol（HDL-C）, supemxide dismutase（SOD）, malondialdehyde （MDA）, nitri oxide（NO） and the injured degree of pancreatic islet. Effects of PDM on the injured human umbilical vein endothelial cell lines（ECV304） induced by H2O2 were also investigated,Result： PDM showed no any significant effect on FSG in normal mice. However, in the mice with diabetes induced by alloxan PDM could remarkably decrease serum glucose tolerance, the contents of FSG,GSP, TC, TG and IDL-C and significantly increased the ratio of HDL-C/TC, the activity of SOD and the concentration of NO. The damage of pancreatic islet induced by alloxan was also significantly attenuated by PDM. Furthermore, PDM promoted the viability of injured ECV304, elevated SOD level and reduced the contents of MDA. Conclusion： results in the present study suggest that PDM can significantly attenuate hypertipidemia and hyperglycemia in diabetic mice, which are probably due to its effects of antioxidation and amelioration of damaged pancreatic islet induced by free radicals.