Therapeutic effects of ethanolic extract from the green cocoon shell of silkworm Bombyx mori on type 2 diabetic mice and its hypoglycaemic mechanism.

Diabetes mellitus is a clinically complex disease characterized by hyperglycaemia with disturbances in carbohydrate, fat and protein metabolism. The aim of this study was to determine the therapeutic effect of ethanolic extract (EE) from the green cocoon sericin layer of silkworm Bombyx mori on mice with type 2 diabetes mellitus (T2DM) and its hypoglycaemic mechanisms. The results showed that oral EE for 7 weeks had significant ameliorative effects on all the biochemical parameters studied in vivo. The levels of oral glucose tolerance and insulin tolerance were significantly improved. The hypoglycaemic rate in the 350 mg kg-1 high dosage group was 39.38%. The levels of nuclear factor kappa B (NFκB), interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-α) in the high dosage EE-treated group were significantly reduced, while activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were obviously increased. The islet area and the number of insulin-positive beta cells increased significantly in the high dose group. Furthermore, expression levels of insulin receptor (IR), insulin receptor substrate (IRS), phosphatidylinositide 3-kinase (PI3K), p-Akt and phospho-glycogen synthase kinase-3β (p-GSK3β) involved in insulin signalling were increased. Adenosine 5'-monophosphate-activated protein kinase (AMPK) and glucose transporter 4 (GLUT4) also were activated to regulate glucose metabolism in EE-treated groups. The levels of glucose 6-phosphatase (G6pase) and phosphoenolpyruvate carboxykinase (PEPCK) decreased, while the glucokinase (GK) level increased to promote glycolysis. The results clearly indicated that oral EE, especially at a high dose, could improve the glucose metabolism of T2DM by reducing inflammatory reactions, enhancing the antioxidant capacity and insulin sensitivity, and regulating the balance between glycolysis and gluconeogenesis, which means that EE has potential ameliorative effects on T2DM mice.