scholarly journals Canagliflozin, a sodium–glucose cotransporter 2 inhibitor, normalizes renal susceptibility to type 1 cardiorenal syndrome through reduction of renal oxidative stress in diabetic rats

2019 ◽  
Vol 10 (4) ◽  
pp. 933-946 ◽  
Author(s):  
Yukishige Kimura ◽  
Atsushi Kuno ◽  
Masaya Tanno ◽  
Tatsuya Sato ◽  
Kouhei Ohno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiorenal Syndrome ◽  
Diabetic Rats ◽  
Sodium Glucose Cotransporter

scholarly journals Beneficial Effect of Aqueous Garlic Extract on Inflammation and Oxidative Stress Status in the Kidneys of Type 1 Diabetic Rats

2016 ◽  
Vol 32 (3) ◽  
pp. 329-336 ◽  
Author(s):  
Abolfazl Nasiri ◽  
Nasrin Ziamajidi ◽  
Roghayeh Abbasalipourkabir ◽  
Mohammad Taghi Goodarzi ◽  
Massoud Saidijam ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Beneficial Effect ◽  
Diabetic Rats ◽  
Garlic Extract ◽  
Oxidative Stress Status ◽  
And Oxidative Stress

scholarly journals Oxidative Stress: Dual Pathway Induction in Cardiorenal Syndrome Type 1 Pathogenesis

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Grazia Maria Virzì ◽  
Anna Clementi ◽  
Massimo de Cal ◽  
Alessandra Brocca ◽  
Sonya Day ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Syndrome Type ◽  
Copper Zinc Superoxide Dismutase ◽  
Stress Markers ◽  
Oxidative Stress Pathway ◽  
Significant Augmentation ◽  
Copper Zinc

Cardiorenal Syndrome Type 1 (Type 1) is a specific condition which is characterized by a rapid worsening of cardiac function leading to acute kidney injury (AKI). Even though its pathophysiology is complex and not still completely understood, oxidative stress seems to play a pivotal role. In this study, we examined the putative role of oxidative stress in the pathogenesis of CRS Type 1. Twenty-three patients with acute heart failure (AHF) were included in the study. Subsequently, 11 patients who developed AKI due to AHF were classified as CRS Type 1. Quantitative determinations for IL-6, myeloperoxidase (MPO), nitric oxide (NO), copper/zinc superoxide dismutase (Cu/ZnSOD), and endogenous peroxidase activity (EPA) were performed. CRS Type 1 patients displayed significant augmentation in circulating ROS and RNS, as well as expression of IL-6. Quantitative analysis of all oxidative stress markers showed significantly lower oxidative stress levels in controls and AHF compared to CRS Type 1 patients (P<0.05). This pilot study demonstrates the significantly heightened presence of dual oxidative stress pathway induction in CRS Type 1 compared to AHF patients. Our findings indicate that oxidative stress is a potential therapeutic target, as it promotes inflammation by ROS/RNS-linked pathogenesis.

scholarly journals Curcumin attenuates oxidative stress in liver in Type 1 diabetic rats

2017 ◽  
Vol 12 (1) ◽  
pp. 452-459 ◽  
Author(s):  
Zhenglu Xie ◽  
Xinqi Zeng ◽  
Xiaqing Li ◽  
Binbin Wu ◽  
Guozhi Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Polyol Pathway ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Curcumin Treatment ◽  
Kinase C ◽  
Diabetic Model ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Plasma Malondialdehyde

AbstractWe investigated the effect of curcumin on liver anti-oxidative stress in the type 1 diabetic rat model induced by streptozotocin (STZ). Experimental diabetic rats were induced by STZ intraperitoneally. All rats were fed for 21 days including three groups of control (NC), diabetic model (DC) and curcumin-treated (Cur, 1.5 g/kg by gavage). The results showed that curcumin-treatment significantly decreased the blood glucose and plasma malondialdehyde levels, but significantly increased the plasma superoxide dismutase, glutathione peroxidase and reduced glutathione levels. Curcumin treatment decreased the activity of aldose reductase, but increased the plasma glucose-6-phosphate dehydrogenase, glucose synthetase and glucose-polymerizing activities. Curcumin treatment significantly decreased the protein of protein kinase C (PKC) and poly ADP ribose polymerase (PARP) expression in the Cur group compared with the DC group. Moreover, the sorbitol dehydrogenase activity was significantly decreased and deterred glucose enters into the polyol pathway leading to an increased NADPH content in the Cur group compared with the DC group. Our data provides evidence that oxidative stress in diabetic rats may be attenuated by curcumin by inhibiting polyol pathway associated with down-regulated expression of PKC and PARP, as evidenced by both an increase the antioxidant enzymes levels and glycogen biosynthesis enzymes activities.

scholarly journals Adeno-Associated Viral Transfer of Glyoxalase-1 Blunts Carbonyl and Oxidative Stresses in Hearts of Type 1 Diabetic Rats

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 592
Author(s):  
Fadhel A. Alomar ◽  
Abdullah Al-Rubaish ◽  
Fahad Al-Muhanna ◽  
Amein K. Al-Ali ◽  
JoEllyn McMillan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ventricular Myocytes ◽  
Diabetic Rats ◽  
Confocal Imaging ◽  
Glyoxalase 1 ◽  
Microvascular Leakage ◽  
Oxidative Stresses ◽  
Rat Hearts ◽  
Longitudinal Strains

Accumulation of methylglyoxal (MG) arising from downregulation of its primary degrading enzyme glyoxalase-1 (Glo1) is an underlying cause of diabetic cardiomyopathy (DC). This study investigated if expressing Glo1 in rat hearts shortly after the onset of Type 1 diabetes mellitus (T1DM) would blunt the development of DC employing the streptozotocin-induced T1DM rat model, an adeno-associated virus containing Glo1 driven by the endothelin-1 promoter (AAV2/9-Endo-Glo1), echocardiography, video edge, confocal imaging, and biochemical/histopathological assays. After eight weeks of T1DM, rats developed DC characterized by a decreased E:A ratio, fractional shortening, and ejection fraction, and increased isovolumetric relaxation time, E: e’ ratio, and circumferential and longitudinal strains. Evoked Ca2+ transients and contractile kinetics were also impaired in ventricular myocytes. Hearts from eight weeks T1DM rats had lower Glo1 and GSH levels, elevated carbonyl/oxidative stress, microvascular leakage, inflammation, and fibrosis. A single injection of AAV2/9 Endo-Glo1 (1.7 × 1012 viron particles/kg) one week after onset of T1DM, potentiated GSH, and blunted MG accumulation, carbonyl/oxidative stress, microvascular leakage, inflammation, fibrosis, and impairments in cardiac and myocyte functions that develop after eight weeks of T1DM. These new data indicate that preventing Glo1 downregulation by administering AAV2/9-Endo-Glo1 to rats one week after the onset of T1DM, blunted the DC that develops after eight weeks of diabetes by attenuating carbonyl/oxidative stresses, microvascular leakage, inflammation, and fibrosis.

Diosmin ameliorates the effects of oxidative stress in lenses of streptozotocin-induced type 1 diabetic rats

2017 ◽  
Vol 69 (5) ◽  
pp. 995-1000 ◽  
Author(s):  
Weronika Wojnar ◽  
Ilona Kaczmarczyk-Sedlak ◽  
Maria Zych
Keyword(s):  
Oxidative Stress ◽  
Diabetic Rats

Testosterone promotes glucose intolerance, lipid disorder and oxidative stress in type 1 diabetic rats

2014 ◽  
Vol 25 (1) ◽  
Author(s):  
Ayodele Olufemi Morakinyo ◽  
Daniel Abiodun Adekunbi ◽  
Kayode Akanni Dada ◽  
Olufeyi Adefunke Adegoke
Keyword(s):  
Oxidative Stress ◽  
Glucose Intolerance ◽  
Diabetic Rats ◽  
Lipid Disorder ◽  
And Oxidative Stress

scholarly journals Dalteparin as a Novel Therapeutic Agent to Prevent Diabetic Encephalopathy by Targeting Oxidative Stress and Inflammation

2020 ◽  
Vol 11 (6) ◽  
pp. 795-804
Author(s):  
Motahareh Zeinivand ◽  
◽  
Arezo Nahavandi ◽  
Tourandokht Baluchnejadmojarad ◽  
Mehrdad Roghani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Therapeutic Agent ◽  
Diabetic Rats ◽  
Brain Inflammation ◽  
Iron Level ◽  
Hepcidin Expression ◽  
Iron Load ◽  
Y Maze ◽  
Male Wistar Rats

Introduction: Hepcidin is the main modulator of systemic iron metabolism, and its role in the brain has been clarified recently. Studies have shown that hepcidin plays an important role in neuronal iron load and inflammation. This issue is of significance because neuronal iron load and inflammation are pathophysiological processes that are highly linked to neurodegeneration. Moreover, the activity of hepcidin has recently been manipulated to recover the neuronal impairment caused by brain inflammation in animal models. Methods: Streptozotocin (STZ) was used to induce type 1 diabetes. Male Wistar rats (n = 40) with a weight range of 200–250 g were divided into control, diabetic, diabetic + insulin, and diabetic + dalteparin groups. Dalteparin (100 mg/kg IP) and insulin (100 mg/kg SC) were administered for 8 weeks. At the end of the experiment, Y-maze and passive avoidance tasks were carried out. The animals were perfused randomly and their hippocampal tissue was isolated for the analysis of markers such as lipid peroxidation like Malondialdehyde (MDA), hepcidin expression, iron, and ferritin. Blood samples were taken for the measurement of serum inflammatory cytokine Interleukin (IL)-6. Results: The findings indicated that treatment with dalteparin reduced IL-6, MDA, ferritin, and hepcidin expression in diabetic rats compared to treatment with insulin (P<0.05). Moreover, treatment with dalteparin did not decrease the iron level or prevented its decline. Conclusion: Treatment with dalteparin improved the cognitive dysfunctions and symptoms of Alzheimer disease in STZ-induced diabetic rats by appropriately modulating and reducing oxidative stress and neuroinflammation. This may enhance the existing knowledge of therapeutics to reduce cognitive impairment in diabetes and is suggested to be a potential therapeutic agent in diabetes.

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