The current study aimed at investigating the therapeutic effects of rubusoside on type 2 diabetes mellitus (T2DM) mice models as an alternative hypoglycemic candidate drug. T2DM mice models were established with a combination of streptozotocin (STZ) intraperitoneal injection and high-fat diet. After 10 weeks of rubusoside intragastric administration (100, 200 mg/kg/day) to the mice, the body weight, fasting blood glucose, glucose tolerance, and blood lipids were measured. The liver protein expression levels of p-AMPK, GLUT2, GLUT4 and total antioxidant capacity were also investigated. After 10 weeks of rubusoside administration, the levels of blood glucose and lipids were decreased in T2DM mice. Compared with the model group, rubusoside administration significantly decreased the liver mass-to-body weight ratio, upregulated p-AMPK and GLUT4, and downregulated GLUT2 expression levels in the liver. Activities of superoxide dismutase (SOD), catalase (CAT), and gluathione peroxidase (GSH-Px) were increased, and the concentration of malondialdehyde (MDA) was decreased to reduce oxidative stress in the liver. Liver hematoxylin and eosin (H&E) pathological analysis also showed that rubusoside had a protective effect on T2DM mice liver. These results demonstrate that rubusoside could be used as an anti-diabetic candidate drug, and that its hypoglycemic mechanism might be related to the activation of adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) to modulate the expression of GLUT2 and GLUT4. Finally, rubusoside could also increase total antioxidant capacity to protect the liver from oxidative stress.
Background Oxidative stress and inflammation play important roles in the pathogenesis of diabetic nephropathy. Raspberry ketone (RK) is one of the main active substances in raspberry and has a variety of medicinal values. Nevertheless, its protective effect on streptozotocin (STZ)-induced diabetic nephropathy mice has not been reported. In this study, we researched if RK improves oxidative stress and inflammation of STZ-induced diabetic nephropathy mice. Methods The model of diabetic nephropathy mice was established by a single injection of STZ (130 mg/kg). Diabetic nephropathy mice were treated orally with 400 mg/kg/day raspberry ketone extract to eight weeks. The expression levels of serum creatinine (Scr), urine micro-albumin (mALB), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β) and interleukin 6 (IL-6) were measured by Enzyme-linked immunosorbent (ELISA). Renal structural changes were investigated by using animal diagnostic ultrasound system. Results RK obviously ameliorated as observed in the visible decrease levels of serum creatinine (Scr), urine micro-albumin (mALB). Furthermore, RK improved expression levels of antioxidant enzyme markers (GSH-Px, SOD, CAT) and obviously reduced MDA, a product of lipid peroxidation, pro-inflammatory divisors (TNF-α, IL-6, IL-1β) in diabetic nephropathy mice. After treatment with RK, we observed that the size of the kidneys and the damage of renal interstitial of mice were obviously improved, as well as the loss of integrity of basement membrane and the renal interstitial edema in diabetic nephropathy mice by using animal diagnostic ultrasound system. Conclusion This study strongly indicates that raspberry ketone provides a protective effect against STZ-induced diabetic nephropathy in improving oxidative stress and inflammation.
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