汪光军,李九九,何立峰,李彦妮,汪金鑫,贾帅帅,陈文军.黄精多糖预防小鼠糖脂代谢紊乱的作用研究[J].食品安全质量检测学报,2020,11(21):7829-7836 |
黄精多糖预防小鼠糖脂代谢紊乱的作用研究 |
Study on the prevention of glycolipid metabolism disorder in mice by polygonatum sibiricum polysaccharides |
投稿时间:2020-07-14 修订日期:2020-10-20 |
DOI: |
中文关键词: 黄精多糖 糖脂代谢 高脂饮食 保护作用 糖尿病 |
英文关键词:polygonatums ibiricum polysaccharides glycolipid metabolism high fat diet protective effect diabetes |
基金项目:2018年安徽高校自然科学研究项目(KJ2018A0677) |
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中文摘要: |
目的 观察黄精多糖(polygonatum sibiricum polysaccharides, PSP)对C57小鼠糖脂代谢功能的保护作用, 根据中医药治未病的理念初步探讨黄精多糖对小鼠糖尿病的预防作用。方法 对C57小鼠进行黄精多糖灌胃干预, 然后采用高脂饮食联合低剂量链脲佐菌素使小鼠糖脂代谢紊乱, 32只小鼠随机分为正常组、PSP高剂量组(800 mg/kg)、PSP低剂量组(400 mg/kg)与模型组。实验后期测定各组小鼠体重、空腹血糖(fasting blood glucose, FBG)、餐后血糖耐量曲线(oral glucose tolerance test, OGTT)、空腹胰岛素(fasting blood insulin, FINS), 计算胰岛素抵抗指数(homeostasismodel assessment-insulin resistance, HOMA-IR); 检测小鼠血清总胆固醇(total cholesterol, TC)、总甘油三酯(total triglyceride, TG)、高密度脂蛋白(high density lipoprotein, HDL-C)、低密度脂蛋白(low density lipoprotein, LDL-C)以及肝脏TG的含量, 观察肝脏组织油红O染色切片, 利用实时定量逆转录聚合酶链反应测定肝脏组织中磷脂酰肌醇3-激酶(phosphoinositide-3-kinase, PI3K)、蛋白激酶B(protein kinase B, AKT)信号分子的mRNA表达水平。结果 经黄精多糖的灌胃干预后, 与模型组小鼠相比, PSP高剂量组小鼠的体重、FBG、FINS、HOMA-IR、TC、TG、HDL、LDL等代谢指标水平显著性降低(P<0.05), PSP低剂量组小鼠体重、糖耐量曲线面积以及肝脏TG水平显著性降低(P<0.05), 其他代谢指标与模型组无显著性差异, PSP高、低剂量组小鼠肝脏脂质沉积现象明显改善且成剂量依赖性, PSP高剂量能够增强小鼠肝脏组织中PI3K/AKT信号通路中PI3K、AKT分子mRNA的表达水平。结论 黄精多糖的灌胃干预可以有效保护小鼠的糖脂代谢功能, 从而预防小鼠糖尿病的发生发展, 并且该种作用可能与增强PI3K、AKT信号分子的表达水平有关。 |
英文摘要: |
Objective To observe the protective effect of polygonatum sibiricum polysaccharides (PSP) on glucose and lipid metabolism in C57 mice, and to preliminarily study the preventive effect of polygonatum sibiricum polysaccharides (PSP) on diabetes mellitus in mice according to the concept of preventive treatment of disease with traditional Chinese medicine. Methods The C57 mice were treated with polygonatum polysaccharides by gavage, and then a high-fat diet combined with low-dose streptozotocin was used to induce the disorder of glucose and lipid metabolism. 32 mice were randomly divided into the normal group, the high-dose PSP group (800 mg/kg), the low-dose PSP group (400 mg/kg) and the model group. At the end of the experiment, body weight, fasting blood glucose (fasting blood glucose, FBG), postpranational blood glucose tolerance curve (oral glucose tolerance test, OGTT), fasting insulin (fasting blood insulin, FINS) were determined, and homeostasismodel assessment insulin resistance index (homa-ir) were calculated. The contents of serum total cholesterol (total cholesterol, TC), total triglyceride (total triglyceride, TG), high-density lipoprotein (high density lipoprotein, hdl-c), low-density lipoprotein (low density lipoprotein, ldl-c) and liver TG in mice were detected. The liver tissues were observed in oil-red O staining sections. mRNA expression levels of signal molecules involved in phosphatidylinositol 3-kinase (phosphoinositide-3-kinase, PI3K) and protein kinase B (protein kinase B, AKT) pathway in liver tissues were determined by real-time quantitative reverse transcription polymerase chain reaction. Results After polygonatum polysaccharide gavage intervention, compared with model group mice, glucose metabolism indexes of PSP high dose group such as body weight in mice, FBG, FINS, HOMA-IR, TC, TG, HDL, LDL showed a significant decrease (P<0.05), the PSP low dose group mice showed a significant decreased the index of weight, the area os glucose tolerance curve and level of liver TG (P<0.05), while other metabolic indexes had no significant difference from the model group. The lipid deposition in the liver of high-dose and low-dose PSP mice was significantly improved and dose-dependent. High dose of PSP could enhance the mRNA expression level of PI3K and AKT molecules in PI3K/AKT signaling pathway in mouse liver tissue. Conclusion The intragastric intervention of polygonatum sibiricum polysaccharides can effectively protect the function of glycolipid metabolism of mice and prevent the occurrence and development of diabetes in mice. Moreover, this effect may be related to the enhancement of the mRNA expression level of PI3K, AKT signaling molecule. |
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