scholarly journals Moderate exercise training reduces kidney oxidative stress and mortality of hypertensive diabetic rats

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Tatiana Sousa Cunha ◽  
Roberta Hack Mendes ◽  
Mariane Bertagnolli ◽  
Vinícius Viegas ◽  
Cristiano Teixeira Mostarda ◽  
...  
2019 ◽  
Vol 27 (3) ◽  
pp. 269-279
Author(s):  
Irina Camelia Chis ◽  
Mihai Socaciu ◽  
Remus Moldovan ◽  
Simona Clichici

Abstract Hyperglycemia and oxidative stress have a major role in the pathogenesis of diabetic vascular complications. In this study, we investigated the efficacy of combining quercetin treatment with moderate exercise training in reversing diabetes-induced oxidative stress and ultrasound modifications in rat carotid arteries. The diabetic Wistar rats were divided into sedentary groups and trained groups. The trained animals went through a regular moderate exercise by swimming (5 weeks). Some non-diabetic and diabetic rats were daily treated with quercetin (30 mg/kg, for 5 weeks). At the end of the study, the imaging evaluation required to assess the effects of diabetes on carotid arteries was performed by micro-ultrasound (MU). The diabetic rats presented atherosclerotic plaques, with an increase in the echogenicity of the carotid artery wall, carotid intima-media thickness (CIMT), and carotid wall thickness, while the diabetic trained rats treated with quercetin presented normal values of these parameters. Malondialde-hyde (MDA) levels, superoxide dismutase (SOD) antioxidant enzyme activity, reduced glutathione (GSH) levels and the reduced (GSH) to oxidized (GSSG) glutathione ratio were determined in the carotid artery tissue. Diabetes caused elevated MDA levels and a decrease in SOD activity, GSH levels and GSH/GSSG ratio in the carotid artery tissue. Treating diabetic rats with quercetin combined with moderate exercise training reversed all these oxidative stress parameters. Our results show that this combination, quercetin and moderate exercise training, can be a good treatment strategy for the vascular complications of diabetes by attenuating hyperglycemia-mediated oxidative stress.


1987 ◽  
Vol 19 (5) ◽  
pp. 497???503 ◽  
Author(s):  
JULIE A. WEGNER ◽  
DONALD D. LUND ◽  
J. MICHAEL OVERTON ◽  
JOHN G. EDWARDS ◽  
ROBERT P. ODA ◽  
...  

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Gobinath Shanmugam ◽  
Madhusudhanan Narasimhan ◽  
Robbie Conley ◽  
Rajesh Kumar Radhakrishnan ◽  
Silvio H Litovsky ◽  
...  

Background: Nuclear erythroid-2 like factor-2 (Nrf2), a master transcriptional regulator of antioxidants, is critical to maintain cellular redox homeostasis. We recently reported that exercise training activates Nrf2/antioxidant signaling in the heart. Isoproterenol (ISO) mediated structural, and functional changes in the heart involve oxidative stress. Here, we tested a hypothesis that moderate exercise training will protect the myocardium from isoproterenol-induced injury by augmenting Nrf2-dependent antioxidant defense system. Methods: Age- and sex-matched WT (C57/BL6) mice (6-8 months old) were subjected to moderate exercise training (MET) on a treadmill for 6 weeks (60 min/day; 10m/min; 0% grade). Randomly assigned untrained (UNT) and trained (MET) animals were intraperitoneally injected (at the start of 6 th week) with 50 mg of isoproterenol/kg.bw./day for 7 consecutive days. MET was continued during ISO administration and the animals (UNT + PBS, UNT + ISO; MET + ISO) underwent echocardiography analysis. Heart tissues were collected for histopathology, Nrf2-ARE promoter binding assay (Active-motif TransAM kit), antioxidant gene (qPCR) and protein (Immunoblotting) levels, and glutathione redox status. Results: ISO administration significantly reduced the Nrf2 promoter activity (p<0.05) and downregulated the expression of cardiac antioxidant genes ( Gclc, Nqo1, Cat, Gsr and Gst-μ ) in UNT mice. Further, increased oxidative stress with severe myocardial injury was evident in UNT+ISO when compared to UNT mice receiving PBS under basal condition. Interestingly, MET stabilized the Nrf2-promoter activity and promoted the expression of Nrf2-dependent antioxidant genes and proteins animals receiving ISO, and thereby attenuated the oxidative stress-induced myocardial damage. Echocardiography analysis showed impaired systolic/diastolic ventricular volumes coupled with decreased cardiac output in UNT+ISO mice, but this was normalized in exercise-trained animals. Conclusion: Thus moderate exercise training conferred protection against ISO-induced myocardial injury by augmentation of Nrf2-antioxidant signaling and attenuation of redox perturbations.


PLoS ONE ◽  
2012 ◽  
Vol 7 (9) ◽  
pp. e45697 ◽  
Author(s):  
Sellamuthu S. Gounder ◽  
Sankaranarayanan Kannan ◽  
Dinesh Devadoss ◽  
Corey J. Miller ◽  
Kevin S. Whitehead ◽  
...  

2015 ◽  
Vol 267 ◽  
pp. 107-114 ◽  
Author(s):  
HaeJee Yoon ◽  
Vikram Thakur ◽  
Danielle Isham ◽  
Mona Fayad ◽  
Munmun Chattopadhyay

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