玉竹多糖对四氧嘧啶糖尿病大鼠胰岛β细胞损伤的保护作用

Protective Effect of Polygonatum odoratum Polysaccharides on Pancreatic β-cell Damage in Alloxan-induced Diabetes in Rats

目的研究玉竹多糖(PoPs)对实验性糖尿病大鼠胰岛β细胞损伤的保护作用及其机制。方法将四氧嘧啶按180mg/kg一次性腹腔注射诱导实验性糖尿病,给予玉竹多糖干预。观察体重、空腹血糖(FBG)的变化,并检测给药30d后大鼠的血清胰岛素(INS)以及胰腺中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)的水平,取胰腺组织做HE染色观察胰岛损伤情况。结果四氧嘧啶诱导的实验性糖尿病大鼠胰岛细胞存在明显的氧化应激损伤。PoPs呈计量依赖性地改善糖尿病大鼠的体重下降,降低FBG,使胰腺组织MDA含量降低,SOD,GSH-Px,CAT活力增强,HE染色显示胰岛损伤减轻,与糖尿病模型组比较具有明显的统计学差异(P<0.05),但PoPs对INS无明显影响。结论玉竹多糖具有降血糖、抗氧化应激作用,对四氧嘧啶糖尿病大鼠的胰岛β细胞损伤有明显的保护作用。

Objective To evaluate the possible protective effects and mechanism of Polygonatum odoratum polysaccharidcs （PoPs） against β - cell damage in experimental alloxan - induced diabetes in rats. Methods Alloxan was injected intraperitoneally at a single dose of 180mg kg^-1 for induction of diabetes. After oral administration with PoPs30 consecutive days for,the level of body weight,the fasting blood glucose（ FBG）, INS in serum and malondialdehyde（ MDA）, superoxide dismutase （SOD）, glutathione peroxidase （ GSH - Px）, catalase（CAT） contents in pancreatic homogenates were assayed by spectrophotometry. Pancreas samples were stained with hematoxylin - eosin （HE） and examined under a light microscope. Results Alloxan successfully induced experimental diabetes in rats, pancreatic island significantly damaged by oxidative stress. Treatment with PoPs markedly increased body weight, decreased fasting blood glucose levels ; Furthemaore, PoPs significantly blocked the increase of MDA production and increased SOD, GSH - Px, CAT activity in pancreatic homogenates in a dose dependent manner as compared wiht the diabetic control（P 〈 0.05 ）. Histopathological showed that the size and cell number of islets were reduced in diabetic control group and PoPs restored the damage of pancreas tissues in rats with diabetes mellitus. But PoPs had no significant influence on INS in serum. Conclusion PoPs has protective effect on pancreatic β - cell damage and the mecharulm may be related wiht hypoglycemic effect and reduction of oxidative stress in alloxan - induced diabetes in rats.