scholarly journals Enhanced oxidative stress and endothelial dysfunction in streptozotocin-diabetic rats exposed to fine particles

2005 ◽  
Vol 99 (3) ◽  
pp. 335-343 ◽  
Author(s):  
Yu-Chen Lei ◽  
Jing-Shiang Hwang ◽  
Chang-Chuan Chan ◽  
Chung-Te Lee ◽  
Tsun-Jen Cheng
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Fine Particles ◽  
Diabetic Rats ◽  
Streptozotocin Diabetic Rats

scholarly journals Fenofibrate Treatment Enhances Antioxidant Status and Attenuates Endothelial Dysfunction in Streptozotocin-Induced Diabetic Rats

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Murat Olukman ◽  
Ebru Demirel Sezer ◽  
Sibel Ülker ◽  
Eser Y. Sözmen ◽  
Gülcihan Mehtap Çınar
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Thiobarbituric Acid ◽  
Diabetic Rats ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Fenofibrate Treatment ◽  
Streptozotocin Diabetic Rats ◽  
Total Homocysteine ◽  
Necrosis Factor

Diabetic endothelial dysfunction is accompanied by increased oxidative stress and upregulated proinflammatory and inflammatory mediators in the vasculature. Activation of peroxisome proliferator-activated receptor-alpha (PPAR-α) results in antioxidant and anti-inflammatory effects. This study was designed to investigate the effect of fenofibrate, a PPAR-αactivator, on the endothelial dysfunction, oxidative stress, and inflammation in streptozotocin diabetic rats. Diabetic rats received fenofibrate (150 mg kg−1day−1) for 4 weeks. Fenofibrate treatment restored the impaired endothelium-dependent relaxation and increased basal nitric oxide availability in diabetic aorta, enhanced erythrocyte/liver superoxide dismutase and catalase levels, ameliorated the abnormal serum/aortic thiobarbituric acid reactive substances, and prevented the increased aortic myeloperoxidase without a significant change in serum total cholesterol and triglyceride levels. It did not affect the decreased total homocysteine level and the increased tumor necrosis factor-αlevel in the serum of diabetic rats. Fenofibrate-induced prevention of the endothelial function seems to be related to its potential antioxidant and antiinflammatory activity.

scholarly journals Hydrogen Peroxide-Induced Inhibition of Vasomotor Activity: Evaluation of Single and Combined Treatments With Vitamin A and Insulin in Streptozotocin-Diabetic Rats

2002 ◽  
Vol 3 (2) ◽  
pp. 119-130 ◽  
Author(s):  
Fulya Zobali ◽  
Tanju Besler ◽  
Nuray Ari ◽  
Çimen Karasu
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Vitamin A ◽  
Diabetic Rats ◽  
Thiobarbituric Acid Reactive Substance ◽  
Single Treatment ◽  
Combined Treatments ◽  
Retinol Metabolism ◽  
Vasomotor Activity ◽  
Streptozotocin Diabetic Rats

A positive correlation has been established between increased oxidative stress and cardiovascular diseases in diabetes mellitus. We evaluated the effects of single or combined treatments with vitamin A (retinol acetate, 30 mg/kg/day, for 12-weeks) and insulin (8-10 IU/rat/day for the final 6-week) on vasomotor activity, oxidative stress and retinol metabolism in 12-week streptozotocin diabetic rats. The vasomotor activity was determined by measuring invitroresponsiveness of aorta rings to phenylephrine (PE) and acetylcholine (ACh) in the absence or in the presence of hydrogen peroxide (H2O2). Preincubation withH2O2(10 μM) produced a significant decrease in PE (1 mM)-induced contraction in untreated-diabetic but not in control rats. Single treatment with insulin counteracted this effect ofH2O2and also reversed the increased contractile response of diabetic aorta to PE, while vitamin A was found to be ineffective.H2O2(10 μM) also inhibited ACh (1 mM)-stimulated endothelium- dependent relaxation two fold more in diabetic than in control aorta. In the prevention ofH2O2-induced inhibition of vascular relaxation to ACh, vitamin A alone was markedly effective while insulin alone was not. The combination of vitamin A plus insulin removed the inhibitory action ofH2O2in diabetic aorta. Diabetic animals displayed an increased level of aorta thiobarbituric acid reactive substance (TBARS) in association with decreased levels of plasma retinol and retinol-binding protein (RBP). Single treatment with insulin, in spite of allowing recovery of normal growth rate and improved glucose and retinol metabolism in diabetic rats, was unable to control TBARS production to the same extent as vitamin A alone. Our findings suggest that the maintenance of ACh-stimulated endothelium-dependent vasorelaxant tone in normal physiological levels depends largely on the prevention and/or inhibition of peroxidative stress, which is achieved by combined treatment with vitamin A plus insulin. The use of vitamin A together with insulin provides a better metabolic control and more benefits than use of insulin alone in the reduction of diabetes-induced vascular complications.

scholarly journals Oxidative Stress in Rats After 60 Days of Hypergalactosemia or Hyperglycemia

2003 ◽  
Vol 22 (6) ◽  
pp. 423-427 ◽  
Author(s):  
Mary Otsyula ◽  
Matthew S. King ◽  
Tonya G. Ketcham ◽  
Ruth A. Sanders ◽  
John B. Watkins
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Glutathione Disulfide ◽  
Hepatic Lipid Peroxidation ◽  
Streptozotocin Diabetic Rats

Two of the models used in current diabetes research include the hypergalactosemic rat and the hyperglucosemic, streptozotocin-induced diabetic rat. Few studies, however, have examined the concurrence of these two models regarding the effects of elevated hexoses on biomarkers of oxidative stress. This study compared the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase and the concentrations of glutathione, glutathione disulfide, and thiobarbituric acid reactants (as a measure of lipid peroxidation) in liver, kidney, and heart of Sprague-Dawley rats after 60 days of either a 50% galactose diet or insulin deficiency caused by streptozotocin injection. Most rats from both models developed bilateral cataracts. Blood glucose and glycosy-lated hemoglobin A1c concentrations were elevated in streptozotocin diabetic rats. Streptozotocin diabetic rats exhibited elevated activities of renal superoxide dismutase, cardiac catalase, and renal and cardiac glutathione peroxidase, as well as elevated hepatic lipid peroxidation. Insulin treatment of streptozotocin-induced diabetic rats normalized altered markers. In galactosemic rats, hepatic lipid peroxidation was increased whereas glutathione reductase activity was diminished. Glutathione levels in liver were decreased in diabetic rats but elevated in the galactosemic rats, whereas hepatic glutathione disulfide concentrations were decreased much more in diabetes than in galactosemia. Insulin treatment reversed/prevented all changes caused by streptozotocin-induced diabetes. Lack of concomitance in these data indicate that the 60-day galactose-fed rat is not experiencing the same oxidative stress as the streptozotocin diabetic rat, and that investigators must be cautious drawing conclusions regarding the concurrence of the effects of the two animal models on oxidative stress biomarkers.

Effects of chronic insulin on endothelial dysfunction of basilar arteries from established streptozotocin-diabetic rats

2004 ◽  
Vol 504 (1-2) ◽  
pp. 119-127 ◽  
Author(s):  
Takayuki Matsumoto ◽  
Shintaro Yoshiyama ◽  
Kentaro Wakabayashi ◽  
Tsuneo Kobayashi ◽  
Katsuo Kamata
Keyword(s):  
Endothelial Dysfunction ◽  
Diabetic Rats ◽  
Basilar Arteries ◽  
Streptozotocin Diabetic Rats

Effects of dietary iron restriction on kidney mitochondria function and oxidative stress in streptozotocin-diabetic rats

Mitochondrion ◽  
2020 ◽  
Vol 54 ◽  
pp. 41-48
Author(s):  
Donovan J. Peña-Montes ◽  
Maribel Huerta-Cervantes ◽  
Mónica Ríos-Silva ◽  
Xóchitl Trujillo ◽  
Christian Cortés-Rojo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Rats ◽  
Dietary Iron ◽  
Kidney Mitochondria ◽  
Iron Restriction ◽  
Streptozotocin Diabetic Rats ◽  
And Oxidative Stress

scholarly journals Ocular Application of the Kinin B1 Receptor Antagonist LF22-0542 Inhibits Retinal Inflammation and Oxidative Stress in Streptozotocin-Diabetic Rats

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e33864 ◽  
Author(s):  
Mylène Pouliot ◽  
Sébastien Talbot ◽  
Jacques Sénécal ◽  
Florence Dotigny ◽  
Elvire Vaucher ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Receptor Antagonist ◽  
Diabetic Rats ◽  
B1 Receptor ◽  
Kinin B1 Receptor ◽  
Streptozotocin Diabetic Rats ◽  
Retinal Inflammation ◽  
And Oxidative Stress

scholarly journals Effects of Ilex Guayusa Tea on Glycaemia, Cardiovascular Autonomic Modulation and Oxidative Stress in Streptozotocin‐Diabetic Rats

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Filipe Fernandes Stoyell‐Conti ◽  
Tafne C. Mello ◽  
Danielle S. Dias ◽  
Nathalia Bernardes ◽  
Amanda A. Araujo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Rats ◽  
Autonomic Modulation ◽  
Streptozotocin Diabetic Rats ◽  
And Oxidative Stress

Abstract 412: The Sodium-Glucose Cotransporter 2 Inhibitor Empagliflozin Improves Diabetic Complications in the Streptozotocin Type 1 Diabetes Mellitus Model by Interfering With Glucotoxicity and Rescue of Beta-Cell Function

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Philipp Welschof ◽  
Matthias Oelze ◽  
Swenja Kröller-Schön ◽  
Thomas Jansen ◽  
Michael Hausding ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Type I Diabetes ◽  
Cardiovascular Complications ◽  
Diabetic Rats ◽  
Low Grade ◽  
Type I ◽  
Urinary Glucose ◽  
And Oxidative Stress

Objectives: In diabetes, cardiovascular complications are associated with endothelial dysfunction and oxidative stress. Empagliflozin (Empa), as a selective sodium-glucose co-transporter 2 inhibitor (SGLT2i) in clinical development, offers a promising novel approach for the treatment of type 2 diabetes by enhancing urinary glucose excretion. The aim of the present study was to test whether treatment with Empa could improve endothelial dysfunction in type I diabetic rats via reduction of glucotoxicity and associated oxidative stress. Research Design and Methods: Type I diabetes in Wistar rats was induced by an intravenous injection of streptozotocin (60 mg/kg). One week after injection Empa was administered via drinking water for 7 weeks. Results: Treatment with Empa (10 and 30 mg/kg/d), showed reduction of blood glucose and a normalization of endothelial dysfunction (aortic rings) in diabetic rats and a reduced oxidative stress in aortic vessels (dihydroethidine staining) and in blood (phorbol ester/zymosan A-stimulated chemiluminescence). Additionally, the pro-inflammatory phenotype and glucotoxicity in diabetic animals was normalized by SGLT2i therapy. Conclusion: In this study we could demonstrate that Empa improves hyperglycemia and prevents the development of endothelial dysfunction and oxidative stress in type 1 diabetic rats. Future studies will investigate the underlying mechanisms of these antioxidant and anti-inflammatory effects with special emphasis on low-grade inflammation, glucotoxicity and oxidative stress, all of which contributes to cardiovascular complications.

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