Oxidative Stress and Cardiac Microvascular Structure in Ischemia and Reperfusion: The Protective Effect of Antioxidant Vitamins

2002 ◽  
Vol 64 (2) ◽  
pp. 265-277 ◽  
Author(s):  
Catherine A. Molyneux ◽  
Matthew C. Glyn ◽  
Barbara J. Ward
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Antioxidant Vitamins ◽  
Ischemia And Reperfusion

Protective Effect of Diphenyl Diselenide on Ischemia and Reperfusion-Induced Cerebral Injury: Involvement of Oxidative Stress and Pro-Inflammatory Cytokines

2012 ◽  
Vol 37 (10) ◽  
pp. 2249-2258 ◽  
Author(s):  
César A. Brüning ◽  
Marina Prigol ◽  
Cristiane Luchese ◽  
Cristiano R. Jesse ◽  
Marta M. M. F. Duarte ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Inflammatory Cytokines ◽  
Cerebral Injury ◽  
Ischemia And Reperfusion ◽  
Diphenyl Diselenide ◽  
Pro Inflammatory Cytokines

scholarly journals Glutathione S-Transferase and Clusterin, New Players in the Ischemic Preconditioning Renal Protection in a Murine Model of Ischemia and Reperfusion

2021 ◽  
Vol 55 (5) ◽  
pp. 635-650
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Ischemic Preconditioning ◽  
Renal Ischemia ◽  
Kidney Cortex ◽  
Ischemia And Reperfusion ◽  
Glutathione S Transferase ◽  
Kidney Medulla ◽  
Qrt Pcr ◽  
Gst Activity

BACKGROUND/AIMS: Renal ischemia and reperfusion injury (IRI) involves oxidative stress, disruption of microvasculature due to endothelial cell damage, loss of epithelial cell polarity secondary to cytoskeletal alterations, inflammation, and the subsequent transition into a mesenchymal phenotype. Ischemic preconditioning (IPC) has been proposed as a therapeutic strategy to avoid/ameliorate the IRI. Since previous results showed that IPC could have differential effects in kidney cortex vs. kidney medulla, in the present study we analyzed the effectiveness and molecular mechanisms implicated in IPC in both kidney regions. METHODS: We evaluated 3 experimental groups of BALB/c male mice: control (sham surgery); renal ischemia (30 min) by bilateral occlusion of the renal pedicle and reperfusion (48 hours) (I/R); and renal IPC (two cycles of 5 min of ischemia and 5 min of reperfusion) applied just before I/R. Acute kidney injury was evaluated by glomerular filtration rate (GFR), Neutrophil Gelatinase-Associated Lipocalin (NGAL) blood level, and histologic analysis. Oxidative stress was studied measurement the Glutathione S-Transferase (GST) activity, GSH/GSSG ratio, and lipoperoxidation levels. Inflammatory mediators (IL-1β, IL-6, Foxp3, and IL-10) were quantified by qRT-PCR. The endothelial (PECAM-1), epithelial (AQP-1), mesenchymal (Vimentin, Fascin, and Hsp47), iNOS, clusterin, and Hsp27 expression were evaluated (qRT-PCR and/or Western blot). RESULTS: The IPC protocol prevented the decrease of GFR, reduced the plasma NGAL, and ameliorated morphological damage in the kidney cortex after I/R. The IPC also prevented the downregulation of GST activity, lipoperoxidation and ameliorated the oxidized glutathione. In addition, IPC prevented the upregulation of vimentin, fascin, and Hsp47, which was associated with the prevention of the downregulation of AQP1 after I/R. The protective effect of IPC was associated with the upregulation of Hsp27, Foxp3, and IL-10 expression in the renal cortex. However, the upregulation of iNOS, IL-1β, IL-6, and clusterin by I/R were not modified by IPC. CONCLUSION: IPC conferred better protection in the kidney cortex as compared to the kidney medulla. The protective effect of IPC was associated with amelioration of oxidative stress, tubular damage, and the induction of markers of Treg lymphocytes activity in the cortical region. Further studies are needed to evaluate if lower tubular cell stress/damage after I/R may explain the preferential induction of Treg response in the kidney cortex induced by IPC.

Antioxidant Activity and Protective Effect against Oxidative Stress on Hippocampal HT22 Cells of Tea Seed Oil

2018 ◽  
Vol 24 (1) ◽  
pp. 53-59
Author(s):  
Jong Min Kim ◽  
Seon Kyeong Park ◽  
Jin Yong Kang ◽  
Seong-kyeong Bae ◽  
Ga-Hee Jeong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Protective Effect ◽  
Seed Oil ◽  
Ht22 Cells ◽  
Tea Seed Oil

Protective effect of DJ-1 against oxidative stress: an advance

2012 ◽  
Vol 32 (1) ◽  
pp. 88-91
Author(s):  
Zhi-yong WANG ◽  
Ling-zhen TANG ◽  
Tian-wen GAO
Keyword(s):  
Oxidative Stress ◽  
Protective Effect

Protective Effect of Swertiamarin on Myocardial Injury Through Activation of Nrf2/HO-1 Pathway in Heart Failure Model of Rats

2020 ◽  
Vol 18 (3) ◽  
pp. 260-265
Author(s):  
Xu Lin ◽  
Zheng Xiaojun ◽  
Lv Heng ◽  
Mo Yipeng ◽  
Tong Hong
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ejection Fraction ◽  
Protective Effect ◽  
Infarct Size ◽  
Rat Model ◽  
Left Ventricular ◽  
Related Factor ◽  
Nuclear Factor ◽  
Internal Dimension

The purpose of this study was to evaluate the protective effect of swertiamarin on heart failure. To this end, a rat model of heart failure was established via left coronary artery ligation. Infarct size of heart tissues was determined using triphenyl tetrazolium chloride staining. Echocardiography was performed to evaluate cardiac function by the determination of ejection fraction, left ventricular internal dimension in diastole and left ventricular internal dimension in systole. The effect of swertiamarin on oxidative stress was evaluated via enzyme-linked immunosorbent assay. The mechanism was evaluated using western blot. Administration of swertiamarin reduced the infarct size of heart tissues in rat models with heart failure. Moreover, swertiamarin treatment ameliorated the cardiac function, increased ejection fraction and fractional shortening, decreased left ventricular internal dimension in diastole and left ventricular internal dimension in systole. Swertiamarin improved oxidative stress with reduced malondialdehyde, while increased superoxide dismutase, glutathione, and GSH peroxidase. Furthermore, nuclear-factor erythroid 2-related factor 2, heme oxygenase and NAD(P)H dehydrogenase (quinone 1) were elevated by swertiamarin treatment in heart tissues of rat model with heart failure. Swertiamarin alleviated heart failure through suppression of oxidative stress response via nuclear-factor erythroid 2-related factor 2/heme oxygenase-1 pathway providing a novel therapeutic strategy for heart failure.

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