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中国精品科技期刊2020
张世奇,王睿,李成良,等. 辣木叶多糖对STZ诱导糖尿病小鼠的降糖效果及其机制[J]. 食品工业科技,2024,45(19):357−365. doi: 10.13386/j.issn1002-0306.2024040369.
引用本文: 张世奇,王睿,李成良,等. 辣木叶多糖对STZ诱导糖尿病小鼠的降糖效果及其机制[J]. 食品工业科技,2024,45(19):357−365. doi: 10.13386/j.issn1002-0306.2024040369.
ZHANG Shiqi, WANG Rui, LI Chengliang, et al. Hypoglycemic Effect of Moringa oleifera Leaf Polysaccharide on STZ-induced Diabetic Mice and Its Mechanism[J]. Science and Technology of Food Industry, 2024, 45(19): 357−365. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2024040369.
Citation: ZHANG Shiqi, WANG Rui, LI Chengliang, et al. Hypoglycemic Effect of Moringa oleifera Leaf Polysaccharide on STZ-induced Diabetic Mice and Its Mechanism[J]. Science and Technology of Food Industry, 2024, 45(19): 357−365. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2024040369.

辣木叶多糖对STZ诱导糖尿病小鼠的降糖效果及其机制

Hypoglycemic Effect of Moringa oleifera Leaf Polysaccharide on STZ-induced Diabetic Mice and Its Mechanism

  • 摘要: 为探讨辣木叶多糖(Moringa oleifera leaf polysaccharide,MOLP)对糖尿病小鼠的降糖效果及其机制,通过建立链脲佐菌素(Streptozotocin,STZ)诱导糖尿病小鼠模型,将实验小鼠设为正常空白组、模型组、MOLP低剂量组(100 mg/kg·bw)、中剂量组(200 mg/kg·bw)、高剂量组(400 mg/kg·bw)和阳性药物组(盐酸二甲双胍200 mg/kg·bw),每组8只,灌胃28 d,测定空腹血糖、血清糖化蛋白、血清胰岛素、肝/肌糖原等生化指标,对肝脏和胰腺中糖代谢关键基因(肝X受体(Liver X Receptor,LXR)、胰腺十二指肠同源异形盒1(Pancreatic duodenal homeobox-1,PDX-1)、葡萄糖激酶(Glucoskinase,GK)、磷酸烯醇丙酮酸羧激酶(Phosphoenolpyruvate carboxykinase,PEPCK)、葡萄糖6磷酸酶(Glucose-6-phosphatase,G6Pase)、葡萄糖转运载体2(Glucose transporter type 2,GLUT2)、胰岛素受体底物1/2(Insulin receptor 1/2,IRS1/2))进行测定,并对各组小鼠肝脏和胰腺组织进行HE染色,观察其组织形态。结果表明:MOLP降糖效果显著,且呈现一定的量效反应关系,MOLP高剂量组(400 mg/kg·bw)的血糖降低水平最为接近阳性药物组,其相关机制为表达显著上调的LXRPDX-1通过调控其下游基因PEPCKG6PaseGKGLUT2IRS1/2 mRNA表达,从而改善糖尿病小鼠的糖代谢紊乱,使其损伤的肝脏组织和胰腺组织得到有效改善,血清胰岛素和肝糖原含量增加,最终达到降血糖作用。

     

    Abstract: To explore the hypoglycemic effect of Moringa oleifera leaf polysaccharide (MOLP) on diabetic mice and its corresponding mechanism, a streptozotocin (STZ)-induced diabetic mouse was modeled. The mice were then divided into groups exposed to low (100 mg/kg·bw), medium (200 mg/kg·bw), and high dosage (400 mg/kg·bw) of MOLP, with a normal blank group, model group and a positive drug group (hydrochloric acid dimethylbiguanide, 200 mg/kg·bw). Eight mice in each group were gavaged for 28 d. Fasting blood glucose, serum glycated protein, serum insulin, hepatic/myocardial glycogen and other biochemical indexes were determined. Additionally, the key genes of glucose metabolism, including liver X receptor (LXR), pancreatic-duodenal homeobox-1 (PDX-1), glucokinase (GK), phosphoenolpyruvate carboxykinase (PEPCK), glucose 6-phosphatase (G6Pase), glucose transporter type 2 (GLUT2) and insulin receptor substrate 1/2 (IRS1/2) were measured in the liver and the pancreas. Furthermore, the mice's liver and pancreas tissues in each group were stained with HE to observe their histomorphology. The results showed that MOLP exhibited a significant hypoglycemic effect and a dose-response relationship. The level of blood glucose reduction in the MOLP high-dose group (400 mg/kg·bw) was closest to that of the positive drug group. The underlying mechanism was that the significantly upregulated expression of LXR and PDX-1 ameliorated the glucose metabolism disorders in diabetic mice by regulating the expression of their downstream genes including PEPCK, G6Pase, GK, GLUT2 and IRS1/2 mRNA. This regulation facilitated the improvement of the damaged liver and pancreatic tissues, increased serum insulin and hepatic glycogen content and ultimately resulted in a hypoglycemic effect.

     

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