scholarly journals Probucol Reduces Testicular Torsion/Detorsion-Induced Ischemia/Reperfusion Injury in Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Si-Ming Wei ◽  
Yu-Min Huang ◽  
Jian Zhou
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Expression ◽  
Testicular Torsion ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Treated Group ◽  
Myeloperoxidase Activity ◽  
Oxygen Species ◽  
Neutrophil Accumulation

This study investigated the effect of probucol, a potent antioxidant, on testicular torsion/detorsion-induced ischemia/reperfusion injury attributable to excess reactive oxygen species released by neutrophils. Sixty male Sprague-Dawley rats were randomly divided into sham-operated control, ischemia-reperfusion, and probucol-treated groups. In the ischemia-reperfusion group, testicular detorsion was performed after 2 hours of left testicular torsion. In the probucol-treated group, after performing the same surgical procedures as in the ischemia-reperfusion group, probucol was given intraperitoneally at testicular detorsion. Orchiectomy was performed to evaluate protein expression of E-selectin which is an endothelial cell adhesion molecule and mediates neutrophil adhesion to vascular endothelium, myeloperoxidase activity (a mark of neutrophil accumulation in the testis), malondialdehyde level (an indicator of reactive oxygen species), and spermatogenesis. E-selectin protein expression, myeloperoxidase activity, and malondialdehyde level were significantly increased, and testicular spermatogenesis was significantly decreased in the ipsilateral testes in the ischemia-reperfusion group, compared with the control group. The probucol-treated group showed significant decreases in E-selectin protein expression, myeloperoxidase activity, and malondialdehyde level and significant increase in testicular spermatogenesis in the ipsilateral testes, compared with the ischemia-reperfusion group. These findings indicate that probucol can protect testicular spermatogenesis by reducing overgeneration of reactive oxygen species by inhibiting E-selectin protein expression and neutrophil accumulation in the testis.

scholarly journals Sesamol Protects Testis from Ischemia-Reperfusion Injury through Scavenging Reactive Oxygen Species and Upregulating CREMτ Expression

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Si-Ming Wei ◽  
Rong-Yun Wang ◽  
Yan-Song Chen
Keyword(s):  
Reactive Oxygen Species ◽  
Reperfusion Injury ◽  
Testicular Torsion ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Control Group ◽  
Oxygen Species ◽  
Germ Cell Differentiation ◽  
Testicular Ischemia

Testicular torsion/detorsion-induced damage is considered as a typical ischemia-reperfusion injury attributed to excessive reactive oxygen species (ROS) production. ROS may regulate many genes whose expression affects cell-cycle regulation, cell proliferation, and apoptosis. The cAMP-responsive element modulator-τ (CREMτ) gene expression in the testis is essential for normal germ cell differentiation. The present study was aimed at investigating the effect of sesamol, a powerful antioxidant, on testicular ischemia-reperfusion injury and related mechanisms in an experimental testicular torsion-detorsion rat model. The type of our study was a randomized controlled trial. Sixty rats were randomly divided into the following 3 groups: (1) sham-operated control group (n=20), (2) testicular ischemia-reperfusion group (n=20), and (3) testicular ischemia-reperfusion+sesamol-treated group (n=20). Testicular ischemia-reperfusion was induced by left testicular torsion (720° rotation in a counterclockwise direction) for 2 hours, followed by detorsion. Orchiectomy was performed at 4 hours or 3 months after detorsion. The testis was obtained for the analysis of the following parameters, including malondialdehyde level (a sensitive indicator of ROS), CREMτ expression, and spermatogenesis. In the testicular ischemia-reperfusion group, the malondialdehyde level was significantly increased with a concomitant significant decrease in CREMτ expression and spermatogenesis in ipsilateral testis. These results suggest that overproduction of ROS after testicular ischemia-reperfusion may downregulate CREMτ expression, which causes spermatogenic injury. Sesamol treatment resulted in a significant reduction in the malondialdehyde level and significant increase in CREMτ expression and spermatogenesis in ipsilateral testis. These data support the above suggestion. Our study shows that sesamol can attenuate testicular ischemia-reperfusion injury through scavenging ROS and upregulating CREMτ expression.

scholarly journals Attenuation Effect of Salvianolic Acid B on Testicular Ischemia-Reperfusion Injury in Rats

2022 ◽  
Vol 2022 ◽  
pp. 1-11
Author(s):  
Si-Ming Wei ◽  
Yu-Min Huang
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Expression ◽  
Xanthine Oxidase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Salvianolic Acid B ◽  
Oxygen Species ◽  
Salvianolic Acid ◽  
Testicular Ischemia

During testicular ischemia-reperfusion, overproduction of reactive oxygen species is associated with testicular injury. We injected hydrogen peroxide (a representative of reactive oxygen species) into normal testis via the testicular artery. The experiment demonstrates that reactive oxygen species can cause spermatogenic injury. Salvianolic acid B, the most abundant bioactive component in Salvia miltiorrhiza Bunge, has been reported to possess a potent antioxidant activity. This study was conducted to evaluate the effect of salvianolic acid B on testicular ischemia-reperfusion injury in a rat testicular torsion-detorsion model. Rats were randomly separated into three groups, including 20 rats in each group: control group with sham operation, testicular ischemia-reperfusion group, and testicular ischemia-reperfusion + salvianolic acid B-treated group. In the testicular ischemia-reperfusion group, left testicular torsion of 720° for 2 hours was induced, and then testicular detorsion was carried out. Rats in the salvianolic acid B-treated group additionally had salvianolic acid B administered intravenously at detorsion. At 4 hours after detorsion, testes of 10 rats from each group were collected to analyze the protein expression of xanthine oxidase which catalyzes generation of reactive oxygen species and malondialdehyde concentration (an indirect indicator of reactive oxygen species). At 3 months after detorsion, testes of the remaining 10 rats from each group were collected to analyze spermatogenesis. Compared with the control group, xanthine oxidase protein expression and malondialdehyde concentration in ipsilateral testes of testicular ischemia-reperfusion group increased significantly, while spermatogenesis decreased significantly. In the salvianolic acid B-treated group, xanthine oxidase protein expression and malondialdehyde concentration in ipsilateral testes decreased significantly, while spermatogenesis increased significantly, compared with the testicular ischemia-reperfusion group. These results suggest that salvianolic acid B can attenuate testicular torsion/detorsion-induced ischemia/reperfusion injury by downregulating the xanthine oxidase protein expression to inhibit reactive oxygen species formation.

scholarly journals Reactive Oxygen Species (ROS)-Activatable Prodrug for Selective Activation of ATF6 after Ischemia/Reperfusion Injury

2019 ◽  
Vol 11 (3) ◽  
pp. 292-297 ◽  
Author(s):  
Jonathan E. Palmer ◽  
Breanna M. Brietske ◽  
Tyler C. Bate ◽  
Erik A. Blackwood ◽  
Manasa Garg ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Selective Activation

scholarly journals Phospholipid oxidation products in ferroptotic myocardial cell death

2019 ◽  
Vol 317 (1) ◽  
pp. H156-H163 ◽  
Author(s):  
Aleksandra Stamenkovic ◽  
Grant N. Pierce ◽  
Amir Ravandi
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Myocardial Cell ◽  
Oxidation Products ◽  
Oxygen Species ◽  
New Therapeutic Approaches

Cell death is an important component of the pathophysiology of any disease. Myocardial disease is no exception. Understanding how and why cells die, particularly in the heart where cardiomyocyte regeneration is limited at best, becomes a critical area of study. Ferroptosis is a recently described form of nonapoptotic cell death. It is an iron-mediated form of cell death that occurs because of accumulation of lipid peroxidation products. Reactive oxygen species and iron-mediated phospholipid peroxidation is a hallmark of ferroptosis. To date, ferroptosis has been shown to be involved in cell death associated with Alzheimer’s disease, Huntington’s disease, cancer, Parkinson’s disease, and kidney degradation. Myocardial reperfusion injury is characterized by iron deposition as well as reactive oxygen species production. These conditions, therefore, favor the induction of ferroptosis. Currently there is no available treatment for reperfusion injury, which accounts for up to 50% of the final infarct size. This review will summarize the evidence that ferroptosis can induce cardiomyocyte death following reperfusion injury and the potential for this knowledge to open new therapeutic approaches for myocardial ischemia-reperfusion injury.

Reactive oxygen species mediate modification of glycocalyx during ischemia-reperfusion injury

2006 ◽  
Vol 290 (6) ◽  
pp. H2247-H2256 ◽  
Author(s):  
Ivan Rubio-Gayosso ◽  
Steven H. Platts ◽  
Brian R. Duling
Keyword(s):  
Reactive Oxygen Species ◽  
Binding Sites ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Control Site ◽  
Oxygen Species ◽  
Heparin Binding ◽  
Heparin Binding Domain

The glycocalyx (Gcx) is a complex and poorly understood structure covering the luminal surface of endothelial cells. It is known to be a determinant of vascular rheology and permeability and may be a key control site for the vascular injuries caused by ischemia-reperfusion (I/R). We used intravital-microscopy to evaluate the effects of I/R injury on two properties of Gcx in mouse cremasteric microvessels: exclusion of macromolecules (anionic-dextrans) and intracapillary distribution of red blood cells (RBC). In this model, the Gcx is rapidly modified by I/R injury with an increase in 70-kDa anionic-dextran penetration without measurable effect on the penetration of 580-kDa anionic-dextran or on RBC exclusion. The effects of I/R injury appear to be mediated by the rapid production of reactive oxygen species (ROS) because they are ameliorated by the addition of exogenous superoxide dismutase-catalase. Intravenous application of allopurinol or heparin also inhibited the effects of I/R injury, and we interpret efficacy of allopurinol as evidence for a role for xanthine-oxidoreductase (XOR) in the response to I/R injury. Heparin, which is hypothesized to displace XOR from a heparin-binding domain in the Gcx, reduced the effects of I/R. The effects of I/R injury were also partially prevented or fully reversed by the intravascular infusion of exogenous hyaluronan. These data demonstrate: 1) the liability of Gcx during I/R injury; 2) the importance of locally produced ROS in the injury to Gcx; and 3) the potential importance of heparin-binding sites in modulating the ROS production. Our findings further highlight the relations between glycosaminoglycans and the pathophysiology of Gcx in vivo.

Intracellular generation of reactive oxygen species in endothelial cells exposed to anoxia-reoxygenation

1997 ◽  
Vol 272 (5) ◽  
pp. L897-L902 ◽  
Author(s):  
J. J. Zulueta ◽  
R. Sawhney ◽  
F. S. Yu ◽  
C. C. Cote ◽  
P. M. Hassoun
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Intracellular Ros ◽  
Ros Formation ◽  
Oxide Synthase

Reactive oxygen species (ROS) play an important role in the pathogenesis of ischemia-reperfusion injury. Extracellular H2O2 generation from bovine pulmonary artery endothelial cells (EC) is known to increase in response to anoxia-reoxygenation (A-R). To determine potential sources of intracellular ROS formation in EC in response to A-R, a fluorometric assay based on the oxidation of 2',7'-dichlorofluorescin was used. Intracellular ROS production declined 40% during 6 h of anoxia (P < 0.05). After A-R, the rates of intracellular ROS formation increased to 148 +/- 9% (P < 0.001) that of normoxic EC (100 +/- 3%). In EC exposed to A-R, allopurinol and NG-methyl-L-arginine (L-NMMA), inhibitors of xanthine oxidase (XO) and nitric oxide synthase (NOS), respectively, reduced intracellular ROS formation by 25 +/- 1% (P < 0.001) and 36 +/- 4% (P < 0.01). Furthermore, at low doses (i.e., 20 microM), deferoxamine and diethylenetriaminepentaacetic acid (DTPA) significantly inhibited intracellular ROS formation. However, at 100 microM, only deferoxamine caused further reduction in DCF fluorescence. In summary, EC respond to A-R by generating increased amounts of XO- and NOS-derived intracellular ROS. The inhibition, to a similar extent, caused by allopurinol and L-NMMA, as well as the effect of deferoxamine and DTPA suggest that the ROS detected is peroxynitrite. Based on these findings and previous work, we conclude that EC generate ROS in response to A-R from at least two different sources: a plasma membrane-bound NADPH oxidase-like enzyme that releases H2O2 extracellularly and XO, which generates intracellular O2-, which in turn may react with nitric oxide to form peroxynitrite.

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