论文部分内容阅读
目的利用四氧嘧啶建立糖尿病小鼠模型,研究蛋白多糖F-苷肽(F-GC)对糖尿病小鼠血糖及肝、肾抗氧化功能的影响。方法昆明小鼠禁食24h后,尾静脉注射42.5mg·kg-1四氧嘧啶生理氯化钠溶液,5~7d后选择空腹血糖大于16.7mmol·L-1的小鼠为造模成功者。随机分为5组,连续ig给药30d,F-苷肽小、中、大剂量组ig剂量分别为0.3、1、3g·kg-1,阳性药物二甲双胍组ig剂量为0.2g·kg-1,模型组与对照组ig等剂量生理氯化钠溶液。给药结束时测血糖,血清胰岛素;取肝、肾组织测抗氧化酶活性以及肝脏糖元含量。结果糖尿病小鼠igF-苷肽30d后,小、中、大剂量组血糖分别下降为8.14%、11.5%、14.68%,呈现一定的剂量效应关系;F-苷肽各组肝、肾超氧化物歧化酶(SOD)活性与模型组相比有显著提高(P<0.05),与阳性药物二甲双胍组比较也显著提高(P<0.05)。F-GC中、高剂量组的肾谷胱甘肽过氧化物酶(GSH-px)活性与模型组比较有显著提高(P<0.01),其中F-GC中、大剂量组提高GSH-px活性的能力较二甲双胍强(P<0.05)。肝GSH-px活性组间无显著变化。结论F-苷肽对四氧嘧啶诱导的糖尿病小鼠有一定降血糖作用,其作用机制与其提高抗氧自由基酶类的活性和保护机体组织免遭过氧化损伤有关。
OBJECTIVE: To establish a diabetic mouse model by using alloxan to study the effect of proteoglycan F-glycoside (F-GC) on blood glucose, anti-oxidative function of liver and kidney in diabetic mice. Methods Kunming mice were fasted for 24 h and then injected intravenously with 42.5 mg · kg-1 alloxan sodium chloride solution. After 5 to 7 days, mice whose fasting blood glucose was greater than 16.7 mmol·L-1 were chosen as successful models. The rats were randomly divided into 5 groups with continuous ig administration for 30 days. The doses of small, medium and large doses of F-glucosidase were 0.3, 1, and 3 g · kg-1, respectively. The dosage of the positive drug metformin was 0.2 g · kg-1 , Model group and control group ig and other doses of physiological sodium chloride solution. At the end of administration, blood glucose and serum insulin were measured. Antioxidase activity and liver glycogen content in liver and kidney tissues were measured. Results After the igF-glycosidic peptide was administered to diabetic mice for 30 days, the blood glucose of small, medium and large dose groups decreased to 8.14%, 11.5% and 14.68%, respectively, showing a dose-dependent effect. The levels of hepatic and renal superoxide Compared with the model group, the activity of dismutase (SOD) was significantly increased (P <0.05), and also significantly increased compared with the positive drug metformin group (P <0.05). The levels of GSH-px in high-dose and high-dose F-GC groups were significantly increased compared with those in model group (P <0.01). In high-dose F-GC group, GSH-px The activity was stronger than metformin (P <0.05). There was no significant change in hepatic GSH-px activity between groups. Conclusion F-glycoside has a hypoglycemic effect on alloxan-induced diabetic mice, and its mechanism may be related to increasing the activity of antioxidant free radical enzymes and protecting the tissues from the damage of peroxidation.