scholarly journals Modulation of potassium currents by angiotensin and oxidative stress in cardiac cells from the diabetic rat

2005 ◽  
Vol 567 (1) ◽  
pp. 177-190 ◽  
Author(s):  
Y. Shimoni ◽  
D. Hunt ◽  
M. Chuang ◽  
K. Y. Chen ◽  
G. Kargacin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Potassium Currents ◽  
Cardiac Cells ◽  
Diabetic Rat ◽  
And Oxidative Stress

scholarly journals Liraglutide protects cardiac function in diabetic rats through the PPARα pathway

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Qian Zhang ◽  
Xinhua Xiao ◽  
Jia Zheng ◽  
Ming Li ◽  
Miao Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Cardiac Dysfunction ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Serum Adiponectin ◽  
Diabetic Rat ◽  
Lv Function ◽  
High Dose ◽  
And Oxidative Stress

Increasing evidence shows that diabetes causes cardiac dysfunction. We hypothesized that a glucagon-like peptide-1 (GLP-1) analog, liraglutide, would attenuate cardiac dysfunction in diabetic rats. A total of 24 Sprague–Dawley (SD) rats were divided into two groups fed either a normal diet (normal, n=6) or a high-fat diet (HFD, n=18) for 4 weeks. Then, the HFD rats were injected with streptozotocin (STZ) to create a diabetic rat model. Diabetic rats were divided into three subgroups receiving vehicle (diabetic, n=6), a low dose of liraglutide (Llirag, 0.2 mg/kg/day, n=6), or a high dose of liraglutide (Hlirag, 0.4 mg/kg/day, n=6). Metabolic parameters, systolic blood pressure (SBP), heart rate (HR), left ventricular (LV) function, and whole genome expression of the heart were determined. Diabetic rats developed insulin resistance, increased blood lipid levels and oxidative stress, and impaired LV function, serum adiponectin, nitric oxide (NO). Liraglutide improved insulin resistance, serum adiponectin, NO, HR, and LV function and reduced blood triglyceride (TG), total cholesterol (TC) levels, and oxidative stress. Moreover, liraglutide increased heart nuclear receptor subfamily 1, group H, member 3 (Nr1h3), peroxisome proliferator activated receptor (Ppar) α (Pparα), and Srebp expression and reduced diacylglycerol O-acyltransferase 1 (Dgat) and angiopoietin-like 3 (Angptl3) expression. Liraglutide prevented cardiac dysfunction by activating the PPARα pathway to inhibit Dgat expression and oxidative stress in diabetic rats.

Combined metoprolol and ascorbic acid treatment prevents intrinsic damage to the heart during diabetic cardiomyopathy

2014 ◽  
Vol 92 (10) ◽  
pp. 827-837 ◽  
Author(s):  
Varun Saran ◽  
Vijay Sharma ◽  
Richard Wambolt ◽  
Violet G. Yuen ◽  
Michael Allard ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
Body Mass ◽  
Diabetic Cardiomyopathy ◽  
Rat Heart ◽  
Systolic Dysfunction ◽  
Diabetic Rat ◽  
Metabolic Disturbances ◽  
Β Blocker ◽  
And Oxidative Stress

Metabolic disturbances and oxidative stress have been highlighted as potential causative factors for the development of diabetic cardiomyopathy. The β-blocker metoprolol is known to improve function in the diabetic rat heart and ameliorates the sequelae associated with oxidative stress, without lowering oxidative stress. The antioxidant ascorbic acid is known to improve function in the diabetic rat heart. We tested whether a combination of ascorbic acid and metoprolol treatment would improve function further than each drug individually. Control and streptozotocin-induced diabetic Wistar rats were treated with metoprolol (15 mg·(kg body mass)−1·day−1, via an osmotic pump) and (or) ascorbic acid (1000 mg·(kg body mass)−1·day−1, via their drinking water). To study the effect of treatment on the development of dysfunction, we examined time points before (5 weeks diabetic) and after (7 weeks diabetic) development of overt systolic dysfunction. Echocardiography and working-heart-perfusion were used to assess cardiac function. Blood and tissue samples were collected to assess the severity of disease and oxidative stress. While both drugs improved function, only ascorbic acid had effects on oxidative damage. Combination treatment had a more pronounced improvement in function. Our β-blocker + antioxidant treatment strategy focused on oxidative stress, not diabetes specifically; therefore, it may prove useful in other diseases where oxidative stress contributes to the pathology.

scholarly journals Alterations in Energy Metabolism, Mitochondrial Function and Redox Homeostasis in GK Diabetic Rat Tissues Treated with Aspirin

Life ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 104
Author(s):  
Annie John ◽  
Layla Amiri ◽  
Jasmin Shafarin ◽  
Saeed Tariq ◽  
Ernest Adeghate ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Mitochondrial Function ◽  
Redox Homeostasis ◽  
Diabetic Rats ◽  
Endocrine Function ◽  
Diabetic Rat ◽  
Rat Tissues ◽  
Gk Rats ◽  
And Oxidative Stress

Our recent studies have demonstrated that aspirin treatment prevents inflammatory and oxidative stress-induced alterations in mitochondrial function, improves glucose tolerance and pancreatic endocrine function and preserves tissue-specific glutathione (GSH)-dependent redox homeostasis in Goto-Kakizaki (GK) diabetic rats. In the current study, we have investigated the mechanism of action of aspirin in maintaining mitochondrial bioenergetics and redox metabolism in the liver and kidneys of GK rats. Aspirin reduced the production of reactive oxygen species (ROS) and oxidative stress-induced changes in GSH metabolism. Aspirin treatment also improved mitochondrial respiratory function and energy metabolism, in addition to regulating the expression of cell signaling proteins that were altered in diabetic animals. Ultrastructural electron microscopy studies revealed decreased accumulation of glycogen in the liver of aspirin-treated diabetic rats. Hypertrophic podocytes with irregular fusion of foot processes in the renal glomerulus and detached microvilli, condensed nuclei and degenerated mitochondria observed in the proximal convoluted tubules of GK rats were partially restored by aspirin. These results provide additional evidence to support our previous observation of moderation of diabetic complications by aspirin treatment in GK rats and may have implications for cautious use of aspirin in the therapeutic management of diabetes.

scholarly journals The Effects of the Melatonin Treatment on the Oxidative Stress and Apoptosis in Diabetic Eye and Brain

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Tuğba Gürpınar ◽  
Nuran Ekerbiçer ◽  
Nazan Uysal ◽  
Turgay Barut ◽  
Figen Tarakçı ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Status ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Histopathological Changes ◽  
Melatonin Treatment ◽  
Adult Rats ◽  
Significant Difference ◽  
Immunohistochemical Methods ◽  
And Oxidative Stress

Oxidative stress plays an important role in the development of complications in diabetes mellitus. Antioxidant therapy has been thought to decrease oxidative stress. The objective of the present study was to explore the effects of melatonin (MLT) on oxidative stress in diabetic rat eye and brain tissue by using immunohistochemical methods. Diabetes was induced by streptozotocin, (STZ, 55 mg/kg/i.p) in adult rats. MLT was given 10 mg/kg/i.p once a day for 2 weeks beginning from the sixth week. Six weeks later, rats were divided into three groups: control (CR), STZ-induced diabetic (STZ), and STZ-induced diabetic group received melatonin (STZ+MLT). Although no significant difference was observed with respect to antioxidant status, NOS activity tended to be higher in the untreated diabetic rats than in the treated rats. It was observed that MLT treatment improved the histopathological changes including apoptosis and oxidative stress in brain and eye in diabetic rat.

scholarly journals Bucindolol Modulates Cardiac Remodeling by Attenuating Oxidative Stress in H9c2 Cardiac Cells Exposed to Norepinephrine

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Bruna Gazzi de Lima-Seolin ◽  
Ashley Nemec-Bakk ◽  
Heidi Forsyth ◽  
Stefanie Kirk ◽  
Alex Sander da Rosa Araujo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Signaling Pathways ◽  
Cardiac Remodeling ◽  
Cardiac Cells ◽  
Antagonist Activity ◽  
Pathological Hypertrophy ◽  
Adrenergic Blocker ◽  
Cell Death Signaling ◽  
And Oxidative Stress

The increased circulation of norepinephrine, found in the diseased heart as a result of sympathetic nervous system overactivation, is responsible for its cardiotoxic effects including pathological hypertrophy, cell death, and oxidative stress. Bucindolol is a third generation adrenergic blocker, which acts on the β1 and β2 receptors, and has additional α1 antagonist activity. Thus, the aim of this study was to investigate the action of bucindolol on oxidative stress, hypertrophy, cell survival, and cell death signaling pathways in H9c2 cardiac cells exposed to norepinephrine. H9c2 cells were incubated with 10 μM norepinephrine for 24 h in the presence or absence of bucindolol (10 μM) treatment for 8 h. Western blot was used to determine the expression of proteins for hypertrophy/survival and death signaling pathways. Flow cytometry was used to assess cell death via caspase-3/7 activity and propidium iodide and reactive oxygen species via measuring the fluorescence of CM-H2DCFDA. Norepinephrine exposure resulted in an increase in oxidative stress as well as cell death. This was accompanied by an increased protein expression of LC3B-II/I. The protein kinase B/mammalian target of the rapamycin (Akt/mTOR) pathway which is involved in cardiac remodeling process was activated in response to norepinephrine and was mitigated by bucindolol. In conclusion, bucindolol was able to modulate cardiac remodeling which is mediated by oxidative stress.

1094 CHOLESTASIS INDUCES APOPTOSIS IN MICE CARDIAC CELLS: THE POSSIBLE ROLE OF NO AND OXIDATIVE STRESS

2010 ◽  
Vol 52 ◽  
pp. S423
Author(s):  
H. Shafaroodi ◽  
F. Ebrahimi ◽  
L. Moezi ◽  
M. Hashemi ◽  
Y. Doostar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Cells ◽  
And Oxidative Stress

Curcumin attenuates hyperglycaemia-mediated AMPK activation and oxidative stress in cerebrum of streptozotocin-induced diabetic rat

2011 ◽  
Vol 45 (7) ◽  
pp. 788-795 ◽  
Author(s):  
Arun Prasath Lakshmanan ◽  
Kenichi Watanabe ◽  
Rajarajan A. Thandavarayan ◽  
Flori R. Sari ◽  
Harima Meilei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Rat ◽  
Ampk Activation ◽  
And Oxidative Stress

scholarly journals Sodium-Glucose Cotransporter Inhibition Prevents Oxidative Stress in the Kidney of Diabetic Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Horacio Osorio ◽  
Israel Coronel ◽  
Abraham Arellano ◽  
Ursino Pacheco ◽  
Rocío Bautista ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subcutaneous Administration ◽  
Immunohistochemical Analysis ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Sodium Glucose Cotransporter ◽  
Lower Body Weight ◽  
Sglt2 Inhibition ◽  
Streptozotocin Induced Diabetes ◽  
And Oxidative Stress

The hyperglycemia triggers several chronic diabetic complications mediated by increased oxidative stress that eventually causes diabetic nephropathy. The aim of this study was to examine if the sodium-glucose cotransporter (SGLT2) inhibition prevents the oxidative stress in the kidney of diabetic rats.Methods. The diabetic rat model was established by intraperitoneal injection of streptozotocin (50 mg/kg). The inhibition of SGLT2 was induced by daily subcutaneous administration of phlorizin (0.4 g/kg). Oxidative stress was assessed by catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) activities and by immunohistochemical analysis of 3-nitrotyrosine (3-NT).Results. Streptozotocin-induced diabetes caused hyperglycemia and lower body weight. The CAT activity decreased in cortex and medulla from diabetic rats; in contrast, the GPx activity increased. Furthermore the 3-NT staining of kidney from diabetic rats increased compared to control rats. The inhibition of SGLT2 decreased hyperglycemia. However, significant diuresis and glucosuria remain in diabetic rats. The phlorizin treatment restores the CAT and GPX activities and decreases 3-NT staining.Conclusion. The inhibition of SGLT2 by phlorizin prevents the hyperglycemia and oxidative stress in kidney of diabetic rats, suggesting a prooxidative mechanism related to SGLT2 activity.

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