scholarly journals Oxidative Stress and Lung Ischemia-Reperfusion Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Renata Salatti Ferrari ◽  
Cristiano Feijó Andrade
Keyword(s):  
Oxidative Stress ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Oxygen Species ◽  
Endothelial Cell Injury ◽  
Lung Protection ◽  
Oxygen Poisoning ◽  
The Complement System ◽  
Oxygen Metabolites

Ischemia-reperfusion (IR) injury is directly related to the formation of reactive oxygen species (ROS), endothelial cell injury, increased vascular permeability, and the activation of neutrophils and platelets, cytokines, and the complement system. Several studies have confirmed the destructiveness of the toxic oxygen metabolites produced and their role in the pathophysiology of different processes, such as oxygen poisoning, inflammation, and ischemic injury. Due to the different degrees of tissue damage resulting from the process of ischemia and subsequent reperfusion, several studies in animal models have focused on the prevention of IR injury and methods of lung protection. Lung IR injury has clinical relevance in the setting of lung transplantation and cardiopulmonary bypass, for which the consequences of IR injury may be devastating in critically ill patients.

Cytosolic free Ca2+ and proteolysis in lethal oxidative injury in endothelial cells

1991 ◽  
Vol 261 (5) ◽  
pp. C889-C896 ◽  
Author(s):  
M. D. Geeraerts ◽  
M. F. Ronveaux-Dupal ◽  
J. J. Lemasters ◽  
B. Herman
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Viability ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rapid Onset ◽  
Acetoxymethyl Ester ◽  
Endothelial Cell Injury

Oxygen free radicals (OFR) are thought to mediate ischemia-reperfusion injury to endothelium of heart, lung, brain, liver, and kidney and contribute to development of atherosclerosis, pulmonary O2 toxicity, and adult respiratory distress syndrome. Increased cytosolic free Ca2+ (Cai2+) has been proposed as a mechanism of injury from oxidative stress, yet the pathways by which an increase in Cai2+ may cause OFR-mediated endothelial cell injury remain unknown. Using multiparameter digitized video microscopy and the fluorescent probes, fura-2 acetoxymethyl ester and propidium iodide, we measured Cai2+ and cell viability in human umbilical endothelial cells during oxidative stress with xanthine (50 microM) plus xanthine oxidase (40 mU/ml). Oxidative stress caused a sustained increase in Cai2+ from a resting level of 90-100 nM to near 500 nM, which was preceded by formation of plasma membrane blebs. The increase in Cai2+ was prevented by removal of extracellular Ca2+ (Cao2+). Prevention of the increase in Cai2+ was associated with prolonged cell viability. Readdition of Cao2+ resulted in an immediate large increase in Cai2+ and rapid onset of cell death. The protease inhibitors, leupeptin and pepstatin, delayed the increase in Cai2+ and prolonged cell viability. The results are consistent with the hypothesis that endothelial cell injury due to oxidative stress may be the result of Cai2+ influx and resultant activation of Ca(2+)-dependent proteases.

Endothelial Cell Injury in Cardiovascular Surgery: The Systemic Inflammatory Response11Recent discoveries in the field of vascular biology have led to an expanded understanding of the pathogenesis of many of the immediate and long-term complications of patients undergoing cardiovascular operations and interventional cardiologic procedures. In particular, the vascular endothelium has emerged as the central focus of many of the biologic events that affect the preoperative, operative, and postoperative course of nearly all heart surgery patients. A recurring theme in the study of endothelial cell biology is the crucial role that endothelial cell injury plays in the difficulties that our patients encounter. The deleterious effects of endothelial cell injury are most evident in the acute syndromes of vasospasm, coagulopathy, ischemia/reperfusion injury, and the systemic inflammatory response to cardiopulmonary bypass. In addition, chronic endothelial cell injury contributes to the development of anastomotic narrowing and the progression of atherosclerosis, both of which limit the long-term success of coronary artery bypass grafting. Because of the increasingly recognized role of the endothelium in cardiovascular function there is a tremendous amount of basic science information detailing the response of the endothelium to injury. This is the fifth in a series of seven reviews intended as an introduction to the major topics of endothelial cell biology that are of importance to the practicing cardiothoracic surgeon. In particular, the authors have focused on the role that the endothelium has on the development of vasomotor dysfunction, bleeding and thrombosis, neutrophil-endothelial cell interaction, and obstructive arteriopathy. The aim of these reviews is to provide a concise reference point for cardiothoracic surgeons as they evaluate the ever-accumulating research findings and new therapies that stem from the study of the endothelium in response to the insults encountered in cardiothoracic surgery.Edward D. Verrier, MD

1997 ◽  
Vol 63 (1) ◽  
pp. 277-284 ◽  
Author(s):  
Edward M Boyle, MD ◽  
Timothy H Pohlman, MD ◽  
Marion C Johnson, MD ◽  
Edward D Verrier, MD
Keyword(s):  
Endothelial Cell ◽  
Cell Biology ◽  
Heart Surgery ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Artery Bypass ◽  
Cell Interaction ◽  
Endothelial Cell Injury

scholarly journals Modulatory Effect of Myokines on Reactive Oxygen Species in Ischemia/Reperfusion

2020 ◽  
Vol 21 (24) ◽  
pp. 9382
Author(s):  
Márton Richárd Szabó ◽  
Márton Pipicz ◽  
Tamás Csont ◽  
Csaba Csonka
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Interleukin 7 ◽  
Species Formation

There is a growing body of evidence showing the importance of physical activity against acute ischemic events in various organs. Ischemia/reperfusion injury (I/R) is characterized by tissue damage as a result of restriction and subsequent restoration of blood supply to an organ. Oxidative stress due to increased reactive oxygen species formation and/or insufficient antioxidant defense is considered to play an important role in I/R. Physical activity not only decreases the general risk factors for ischemia but also confers direct anti-ischemic protection via myokine production. Myokines are skeletal muscle-derived cytokines, representing multifunctional communication channels between the contracting skeletal muscle and other organs through an endocrine manner. In this review, we discuss the most prominent members of the myokines (i.e., brain-derived neurotrophic factor (BDNF), cathepsin B, decorin, fibroblast growth factors-2 and -21, follistatin, follistatin-like, insulin-like growth factor-1; interleukin-6, interleukin-7, interleukin-15, irisin, leukemia inhibitory factor, meteorin-like, myonectin, musclin, myostatin, and osteoglycin) with a particular interest in their potential influence on reactive oxygen and nitrogen species formation or antioxidant capacity. A better understanding of the mechanism of action of myokines and particularly their participation in the regulation of oxidative stress may widen their possible therapeutic use and, thereby, may support the fight against I/R.

Diosmetin Ameliorates Cerebral Ischemia/Reperfusion Injury in PC12 Cells Through Nuclear Factor-kB (NF-kB) and Nuclear Factor Erythroid 2-Related Factor/Heme Oxygenase-1 (Nrf 2/HO-1) Pathway

2019 ◽  
Vol 17 (3) ◽  
pp. 322-328
Author(s):  
Luan Lan ◽  
Cao Lanxiu ◽  
Zhu Lei ◽  
Sun Jianhua
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Pc12 Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Diosmetin, a natural flavonoid, exhibits a variety of pharmacologic activities including inhibition of inflammation and oxidation. Therefore, its potential role in the management of cerebral ischemia/reperfusion (I/R) injury remains to be examined. In this study, we explored the underlying molecular mechanisms of diosmetin effects on cerebral ischemia/reperfusion injury in vitro. The results show that hypoxia/reoxygenation treatment of PC12 cells decreased cell viability and increased apoptosis, inflammation and oxidative stress. Diosmetin improved cellular viability, decreased lactate dehydrogenase release, and inhibited apoptosis in hypoxia-/reoxygenation-treated PC12 cells. Furthermore, diosmetin effectively inhibited the NF-kB signaling pathway to attenuate the inflammatory response. Also, diosmetin inhibited reactive oxygen species generation to attenuate I/R injury-induced oxidative stress in PC12 cells probably through the activation of Nrf 2/HO-1 pathway. Therefore, diosmetin effectively protected cells from I/R injury in nerve cells by scavenging reactive oxygen species by activating Nrf 2/HO-1 pathway and inhibiting inflammation by the suppression of NF-kB signaling pathway. Diosmetin can be regarded as a potential agent for cerebral ischemia/reperfusion injury treatment.

scholarly journals Cordycepin protects renal ischemia/reperfusion injury through regulating inflammation, apoptosis, and oxidative stress

2020 ◽  
Vol 52 (2) ◽  
pp. 125-132
Author(s):  
Feng Han ◽  
Meng Dou ◽  
Yuxiang Wang ◽  
Cuixiang Xu ◽  
Yang Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Well Being ◽  
Renal Ischemia ◽  
Cordyceps Sinensis ◽  
Renal Ischemia Reperfusion Injury ◽  
And Oxidative Stress

Abstract Cordycepin (3′-deoxyadenosine) is a naturally occurring adenosine analog and one of the bioactive constituents isolated from Cordyceps sinensis, species of the fungal genus Cordyceps. It has traditionally been a prized Chinese folk medicine for the human well-being. However, the actions of cordycepin against renal ischemia/reperfusion injury (I/R) are still unknown. In the present study, rats were subject to I/R and cordycepin was intragastrically administered for seven consecutive days before surgery to investigate the effects and mechanisms of cordycepin against renal I/R injury. The test results of kidney and peripheral blood samples of experimental animals showed that cordycepin significantly decreased serum blood urea nitrogen and creatinine levels and markedly attenuated cell injury. Mechanistic studies showed that cordycepin significantly regulated inflammation, apoptosis, and oxidative stress. These data provide new insights for investigating the natural product with the nephroprotective effect against I/R, which should be developed as a new therapeutic agent for the treatment of I/R in the future.

scholarly journals Punicalin Alleviates OGD/R-Triggered Cell Injury via TGF-β-Mediated Oxidative Stress and Cell Cycle in Neuroblastoma Cells SH-SY5Y

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Tiansong Yang ◽  
Qingyong Wang ◽  
Yuanyuan Qu ◽  
Yan Liu ◽  
Chuwen Feng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Reperfusion Injury ◽  
Active Component ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Punica Granatum ◽  
Smad Pathway ◽  
Punica Granatum L

Purpose. The research aimed to identify the active component from Punica granatum L. to alleviate ischemia/reperfusion injury and clarify the underlying mechanism of the active component alleviating ischemia/reperfusion injury. Materials and Methods. The SH-SY5Y cell model of oxygen-glucose deprivation/reoxygenation (OGD/R) was established to simulate the ischemia/reperfusion injury. According to the strategy of bioassay-guided isolation, the active component of punicalin from Punica granatum L. was identified. Flow cytometry and Western blotting were employed to evaluate the effects of OGD/R and/or punicalin on cell cycle arrest. Immunofluorescence assay was applied to assess the nucleus translocation. The relative content of ROS and GSH and the enzyme activities of CAT and SOD were examined using ELISA. Results. The data of bioassay-guided isolation showed that punicalin from Punica granatum L. could alleviate OGD/R-induced cell injury in SH-SY5Y cells. Flow cytometry analysis and Western blotting for probing the expression of CDK1, p-CDK1, cyclin B1, and p21 revealed that punicalin could relieve OGD/R-induced cell cycle G0/G1 arrest. Additionally, immunofluorescence assay and Western blotting for probing the expression of TGF-β and p-Smad2/p-Smad3 showed that punicalin could relieve the OGD/R-induced TGF-β/Smad pathway. Furthermore, the TGF-β/Smad pathway inhibitor of LY2157299 was employed to confirm that the TGF-β/Smad pathway is crucial to the effect of punicalin. At last, it was indicated that punicalin could relieve OGD/R-induced oxidative stress. Conclusion. Punicalin, an active component from Punica granatum L., was identified as a protective agent to alleviate the OGD/R-induced cell injury, which could exert the protective effect via TGF-β/Smad pathway-regulated oxidative stress and cell cycle arrest in SH-SY5Y cells.

Characterization of the Protective Effect of Tetrahydrobiopterin Against S-Nitroso-N -Acetyl-D ,L-Penicillamine Induced Endothelial Cell Injury

Pteridines ◽  
1999 ◽  
Vol 10 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Masakazu Ishii ◽  
Shunichi Shimizu ◽  
Kazutaka Momose ◽  
Yuji Kiuchi ◽  
Toshinori Yamamoto
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Protective Effect ◽  
Cell Injury ◽  
Oxygen Species ◽  
No Donor ◽  
Endothelial Cell Injury ◽  
Ros Scavenger ◽  
Intracellular Oxidative Stress

The purpose of this study was to characterize the protective effect of tetrahydrobiopterin (BH4), one of the cofactors of nitric oxide (NO) synthase, against NO-induced endothelial cell injury. The addition of S-nitroso-N-acetyl-D,L-penicillamine (SNAP), a NO donor, to endothelial cells induced the release of lactate dehydrogenase (LDH), a marker for cell injury. The SNAP-induced endothelial cell injury was markedly reduced by pretreatment with sepiapterin, a precursor of BH4 synthesis. On the other hand, exogenous BH4 had little effect on the SNAP-induced endothelial cell injury. We recently found that NO-induced endothelial cell injury involves a part of H202 production, since the injury was blocked by the treatment with catalase. Although BH4 released reactive oxygen species (ROS) in cell-free conditions, the increase in intracellular BH4 by pretreatment with sepiapterin strongly reduced H202-induced intracellular oxidative stress. These findings suggest that the increase in intracellular BH4 content but not extracellular BH4, strongly attenuates NO-induced endothelial cell injury by at least one of the mechanisms by which BH4 reduces H202-induced oxidative stress. Intracellular BH4 seems mainly to play a role as an antioxidant or as a ROS-scavenger.

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