桑叶生物碱对氧化应激小鼠糖脂代谢异常及肝损伤的改善作用

目的:探究桑叶生物碱对氧化应激所致小鼠糖脂代谢异常及肝损伤是否具有改善作用,旨在为桑叶生物碱的深入利用提供理论依据.方法:采用连续20 d腹腔注射1 000 mg/kg mb D-半乳糖建立小鼠氧化损伤模型,分别对造模成功的小鼠灌胃低(50mg/kg mb)、中(100 mg/kg mb)、高(200 mg/kg mb...

Improvement Effect of Mulberry Leaf Alkaloids on Abnormal Glucose and Lipid Metabolism and Liver Injury Induced by Oxidative Stress in Mice

Objective: To explore whether mulberry leaf alkaloids can improve abnormal glucose and lipid metabolism and liver injury induced by oxidative stress in mice for the purpose of provide a theoretical basis for the scientific utilization of mulberry leaves. Methods: A mouse model of oxidative injury was generated by intraperitoneal injection of D-galactose at a dose of 1 000 mg/kg mb for 20 days. Following successful model establishment, the mice were randomly divided into five groups, including model, positive control (200 mg/kg mb of glutathione) and low-, medium- and high-dose mulberry leaf alkaloids (50, 100, and 200 mg/kg mb) groups. The changes of fasting blood glucose, lipid level and liver injury indicators were measured at 0, 4, 8 and 12 weeks of gavage. Results: Compared with the model group, fasting blood glucose, plasma total cholesterol (TC) and triglycerides (TG), and the activities of liver alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were significantly decreased in the positive control group and the medium- and high-dose mulberry leaf alkaloids groups (P < 0.05). Meanwhile, there was no significant difference in all these parameters between the high-dose mulberry leaf alkaloids group and the positive control group, and both treatments restored them to normal, demonstrating that mulberry leaf alkaloids can improve abnormal glucose and lipid metabolism and liver injury in a dose but not time-dependent manner. Histopathological observation showed that the degree of liver lesions in the positive control group and the mulberry alkaloids groups was significantly reduced. Conclusion: Mulberry leaf alkaloids can improve abnormal glucose and lipid metabolism and liver damage caused by oxidative stress, and the underlying mechanism may be related to inhibiting the occurrence and development of oxidative stress.