Conclusion
MDE possesses substantial antidiabetic activity, especially in lipid disorder regulation. This suggests that the use of MDE can be generalized to broader pharmacological studies, such as obesity and hyperlipidaemia.
Methods
Sprague-Dawley rats were fed a high-fat diet for 6 consecutive weeks, followed by intraperitoneal injection of streptozotocin (STZ) (30 mg/kg) to induce diabetes. T2DM rats were divided into untreated diabetic, metformin-treated and MDE-treated groups. Additionally, normal rats without treatment served as the control group (n = 6). Metformin (250 mg/kg) and MDE (600 mg/kg) were intragastrically administered to T2DM rats for 5 consecutive weeks. Serum samples were evaluated via ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UHPLC/QTOF-MS), followed by principal components analysis (PCA) and orthogonal partial least squares discriminant analysis (OPLS-DA).
Objective
To investigate the therapeutic mechanism of MDE in T2DM rats.Materials and
Results
The 17 identified potential biomarkers were mainly involved in lipid, amino acid, arachidonic acid, taurine and nicotinic acid metabolism. MDE also significantly reduced the level of fasting blood glucose (FBG), oral glucose tolerance, insulin, total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), malondialdehyde (MDA), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and urea nitrogen (BUN) in T2DM rats. The high-density lipoprotein (HDL), serum creatinine (Scr), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) levels were elevated in MDE-treated group.