ABSTRACT
Abstract Background and aim: Stingless bee propolis, a resinous compound processed by mandibular secretion of stingless bees, is used for maintenance of hygiene and stability of beehives. Research on stingless bee propolis shows therapeutic properties attributed to polyphenols exhibiting antioxidative, antihyperglycemic and antiischemic effect. However, the cardioprotective effect of stingless bee propolis on diabetic cardiomyopathy is unknown. Methods: Adult male Sprague Dawley rats were randomised to five groups: normal group, diabetic group, diabetic given metformin (DM+M), diabetic given propolis (DM+P) and diabetic given combination therapy (DM+M+P) and treated for four weeks. Body weight, fasting blood glucose, food and water intake were taken weekly. At the end of experiment, biomarkers of oxidative damage were measured in serum and heart tissue. Antioxidants in heart tissue were quantified. Part of left ventricle of heart was processed for histological staining including Haematoxylin and Eosin (H&E) stain for myocyte size and Masson's Trichrome (MT) stain for heart fibrosis and perivascular fibrosis. Results: Propolis alleviated features of diabetic cardiomyopathy such as myocyte hypertrophy, heart fibrosis and perivascular fibrosis associated with improvement in antioxidative status. Conclusion: This study reports beneficial effect of propolis and combination with metformin in alleviating histopathological feature of diabetic cardiomyopathy by modulating antioxidants, making propolis an emerging complementary therapy.
Subject(s)
Animals , Male , Rats , Propolis/adverse effects , Bees/classification , Diabetic Cardiomyopathies/pathology , Staining and Labeling/instrumentation , Blood Glucose/metabolism , Rats, Sprague-Dawley/classification , Cardiomegaly/pathology , Eosine Yellowish-(YS) , Drinking , Heart Ventricles/abnormalities , Hypoglycemic Agents , Metformin/agonists , Antioxidants/adverse effectsABSTRACT
Diabetic nephropathy, the leading cause of end stage renal disease in many countries, is pathologically characterized by glomerular and tubular hypertrophy, extracellular matrix accumulation, inflammatory cell infiltration, and podocytopenia associated with foot process effacement, which eventually results in glomerulosclerosis and tubular atrophy. The pathogenesis of diabetic nephropathy comprises both metabolic and hemodynamic factors related to diabetes. Hemodynamic factors include intraglomerular hypertension which is associated with the activation of both systemic and local renin-angiotensin system. Hyperglycemia per se, advanced glycation end-products and glucose-dependent aldose reductase pathways, as metabolic factors, is also known to contribute to the development and progression of diabetic nephropathy. All of these factors induce various cytokines and activate intracellular signal transduction pathways such as protein kinase C and mitogen-activated protein kinase, ultimately leading to diabetic nephropathy.
Subject(s)
Aldehyde Reductase , Atrophy , Cytokines , Diabetic Nephropathies , Extracellular Matrix , Foot , Hemodynamics , Hyperglycemia , Hypertension , Hypertrophy , Kidney Failure, Chronic , Protein Kinase C , Protein Kinases , Reactive Oxygen Species , Renin-Angiotensin System , Signal TransductionABSTRACT
Diabetic nephropathy, the leading cause of end stage renal disease in many countries, is pathologically characterized by glomerular and tubular hypertrophy, extracellular matrix accumulation, inflammatory cell infiltration, and podocytopenia associated with foot process effacement, which eventually results in glomerulosclerosis and tubular atrophy. The pathogenesis of diabetic nephropathy comprises both metabolic and hemodynamic factors related to diabetes. Hemodynamic factors include intraglomerular hypertension which is associated with the activation of both systemic and local renin-angiotensin system. Hyperglycemia per se, advanced glycation end-products and glucose-dependent aldose reductase pathways, as metabolic factors, is also known to contribute to the development and progression of diabetic nephropathy. All of these factors induce various cytokines and activate intracellular signal transduction pathways such as protein kinase C and mitogen-activated protein kinase, ultimately leading to diabetic nephropathy.