沙棘蛋白的特性及其对db/db糖尿病小鼠的降血糖作用

本文研究了沙棘蛋白对2型糖尿病模型db/db小鼠的降血糖作用。以m/m小鼠为正常对照组,db/db糖尿病模型小鼠为研究对象,每日灌胃300 mg/kg二甲双胍和不同剂量的沙棘蛋白,分别为沙棘蛋白高剂量组(SSPH,200 mg/kg)、沙棘蛋白中剂量组(SSPM,100 mg/kg)、沙棘蛋白低剂量组(SSPL,50 mg/kg),连续灌胃8周。测量初始血糖和体重以及灌胃第1周、第4周、第8周小鼠体重和血糖,并于第8周末对小鼠进行口服糖耐量测试(OGTTs)。db/db小鼠在实验开始时就表现出明显肥胖,行动迟缓,贪食贪饮,高血糖等症状,实验进行4周后,db/db小鼠未治疗组(DC)较沙棘蛋白治疗组体重增长缓慢、小鼠眼神呆滞、毛发稀疏、垫料潮湿。治疗8周后与DC组血糖峰值(28.06 mmol/L)相比SSPL组血糖值为19.89 mmol/L,降血糖效果显著(P<0.05),SSPH体重增加明显,增长率为9.19%,各组小鼠精神状态良好。实验表明沙棘蛋白可以明显降低db/db小鼠的血糖,减轻糖尿病对小鼠的损伤。

Characteristics of Seabuckthorn Seed Protein and Its Hypoglycemic Effect on db/db Diabetic Mice

The hypoglycemic effect of seabuckthorn seed protein on type 2 diabetic model db/db mice was studied. Taking m/m mice as normal control group and db/db diabetic model mice as research objects,Metformin(300 mg/kg)and seabuckthorn seed protein(SSP)were intragastrically administered daily for 8 weeks,includind high dose seabuckthorn seed protein group(SSPH,200 mg/kg),seabuckthorn seed protein medium dose group(SSPM,100 mg/kg)and seabuckthorn seed protein low dose group(SSPL,50 mg/kg). The initial blood sugar and body weight were measured,as well as the body weight and blood sugar of mice in the first,fourth and eighth weeks after gastric administration. The oral glucose tolerance tests(OGTTs)was carried out at the eighth week. db/db mice showed obvious obesity,slow action,gluttony,hyperglycemia and other symptoms at the beginning of the experiment. Four weeks after the experiment,the weight gain of the untreated db/db mice(DC)was slower than that of the SSP treated mice,the glassy eyes,sparse hair and wetter cushion. After 8 weeks of treatment,compared with the peak blood glucose(28.06 mmol/L)of DC group,the blood glucose value of SSPL group was 19.89 mmol/L,showing the significant hypoglycemic effect(P<0.05). The weight of SSPH group increased significantly,9.19% growth rate,and the mice in each group were in good mental state. The results showed that seabuckthorn protein could significantly reduce blood sugar in db/db mice and alleviate the damage of diabetes in mice.