scholarly journals Dietary flaxseed enhances antioxidant defenses and is protective in a mouse model of lung ischemia-reperfusion injury

2008 ◽  
Vol 294 (2) ◽  
pp. L255-L265 ◽  
Author(s):  
James C. Lee ◽  
Faiz Bhora ◽  
Jing Sun ◽  
Guanjun Cheng ◽  
Evguenia Arguiri ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Murine Model ◽  
Ischemia Reperfusion Injury ◽  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
Antioxidant Properties ◽  
Lung Damage ◽  
Antioxidant Defenses ◽  
Ros Generation ◽  
Heme Oxygenase 1

Dietary flaxseed (FS) is a nutritional whole grain with high contents of omega-3 fatty acids and lignans with anti-inflammatory and antioxidant properties. We evaluated FS in a murine model of pulmonary ischemia-reperfusion injury (IRI) by dietary supplementation of 0% (control) or 10% (treatment) FS before IRI. Mice fed 0% FS undergoing IRI had a significant decrease in arterial oxygenation (PaO2) and a significant increase in bronchoalveolar lavage (BAL) protein compared with sham-operated mice. However, mice fed 10% FS undergoing IRI had a significant improvement in both PaO2 and BAL protein compared with mice fed 0% FS undergoing IRI. In addition, oxidative lung damage was decreased in 10% FS-supplemented mice undergoing IRI, as assessed by malondialdehyde levels. Immunohistochemical staining of lungs for iPF2α-III F2 isoprostane, a measure of lipid oxidation, was diminished. FS-supplemented mice had less reactive oxygen species (ROS) release from the vascular endothelium in lungs in an ex vivo model of IRI, and alveolar macrophages isolated from FS-fed mice had significantly reduced ROS generation in response to oxidative burst. Pulmonary microvascular endothelial cells produced less ROS in a flow cessation model of ischemia when preincubated with purified FS lignan metabolites. Pharmacological inhibition of heme oxygenase-1 (HO-1) resulted in only a partial reduction of FS protection in the same model. We conclude that dietary FS is protective against IRI in an experimental murine model and that FS affects ROS generation and ROS detoxification via pathways not limited to upregulation of antioxidant enzymes such as HO-1.

scholarly journals Astragaloside IV Attenuates Myocardial Ischemia-Reperfusion Injury from Oxidative Stress by Regulating Succinate, Lysophospholipid Metabolism, and ROS Scavenging System

2019 ◽  
Vol 2019 ◽  
pp. 1-17 ◽  
Author(s):  
Miaomiao Jiang ◽  
Jingyu Ni ◽  
Yuanlin Cao ◽  
Xiaoxue Xing ◽  
Qian Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
Ros Generation ◽  
Heme Oxygenase 1 ◽  
Ros Scavenging ◽  
Astragaloside Iv ◽  
Wide Range

Astragaloside IV is one of the main active ingredients isolated from Astragalus membranaceus. Here we confirmed its protective effect against cardiac ischemia-reperfusion (I/R) injury and aimed to investigate the potential molecular mechanisms involved. Pretreatment of ex vivo and in vivo I/R-induced rat models by astragaloside IV significantly prevented the ratio of myocardium infarct size, systolic and diastolic dysfunction, and the production of creatine kinase and lactate dehydrogenase. Metabolic analyses showed that I/R injury caused a notable reduction of succinate and elevation of lysophospholipids, indicating excessive reactive oxygen species (ROS) generation driven by succinate’s rapid reoxidization and glycerophospholipid degradation. Molecular validation mechanistically revealed that astragaloside IV stimulated nuclear factor (erythroid-derived 2)-like 2 (Nrf2) released from Kelch-like ECH-associated protein 1 (Keap1) and translocated to the nucleus to combine with musculoaponeurotic fibrosarcoma (Maf) to initiate the transcription of antioxidative gene heme oxygenase-1 (HO-1), which performed a wide range of ROS scavenging processes against pathological oxidative stress in the hearts. As expected, increasing succinate and decreasing lysophospholipid levels were observed in the astragaloside IV-pretreated group compared with the I/R model group. These results suggested that astragaloside IV ameliorated myocardial I/R injury by modulating succinate and lysophospholipid metabolism and scavenging ROS via the Nrf2 signal pathway.

scholarly journals Murine Model of Intestinal Ischemia-reperfusion Injury

10.3791/53881 ◽  
2016 ◽  
Author(s):  
Ekaterina O. Gubernatorova ◽  
Ernesto Perez-Chanona ◽  
Ekaterina P. Koroleva ◽  
Christian Jobin ◽  
Alexei V. Tumanov
Keyword(s):  
Reperfusion Injury ◽  
Murine Model ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

Flaxseed Protects Against the Inflammatory Phase of Lung Ischemia Reperfusion Injury in a Murine Model

2010 ◽  
Vol 158 (2) ◽  
pp. 358
Author(s):  
S.S. Razi ◽  
G. Schwartz ◽  
D. Boone ◽  
X. Li ◽  
S. Belsley ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Murine Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inflammatory Phase

scholarly journals Targeting chronic cardiac remodeling with cardiac progenitor cells in a murine model of ischemia/reperfusion injury

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0173657 ◽  
Author(s):  
Janine C. Deddens ◽  
Dries A. Feyen ◽  
Peter-Paul Zwetsloot ◽  
Maike A. Brans ◽  
Sailay Siddiqi ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Progenitor Cells ◽  
Murine Model ◽  
Cardiac Remodeling ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Progenitor Cells

scholarly journals PR-39, a potent neutrophil inhibitor, attenuates myocardial ischemia-reperfusion injury in mice

2000 ◽  
Vol 279 (6) ◽  
pp. H2824-H2828 ◽  
Author(s):  
Michaela R. Hoffmeyer ◽  
Rosario Scalia ◽  
Chris R. Ross ◽  
Steven P. Jones ◽  
David J. Lefer
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Murine Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Polymorphonuclear Neutrophil ◽  
Leukocyte Rolling ◽  
Rat Mesentery ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

We investigated the effects of PR-39, a recently discovered neutrophil inhibitor, in a murine model of myocardial ischemia-reperfusion injury. Mice were given an intravenous injection of vehicle ( n = 12) or PR-39 ( n = 9) and subjected to 30 min of coronary artery occlusion followed by 24 h of reperfusion. In addition, the effects of PR-39 on leukocyte rolling and adhesion were studied utilizing intravital microscopy of the rat mesentery. The area-at-risk per left ventricle was similar in vehicle- and PR-39-treated mice. However, myocardial infarct per risk area was significantly ( P < 0.01) reduced in PR-39 treated hearts (21.0 ± 3.8%) compared with vehicle (47.1 ± 4.8%). Histological analysis of ischemic reperfused myocardium demonstrated a significant ( P < 0.01) reduction in polymorphonuclear neutrophil (PMN) accumulation in PR-39-treated hearts ( n = 6, 34.3 ± 1.7 PMN/mm2) compared with vehicle-treated myocardium ( n = 6, 59.7 ± 3.1 PMN/mm2). In addition, PR-39 significantly ( P < 0.05) attenuated leukocyte rolling and adherence in rat inflamed mesentery. These results indicate that PR-39 inhibits leukocyte recruitment into inflamed tissue and attenuated myocardial reperfusion injury in a murine model of myocardial ischemia-reperfusion.

scholarly journals Ex vivo carbon monoxide prevents cytochrome P450 degradation and ischemia/reperfusion injury of kidney grafts

2008 ◽  
Vol 74 (8) ◽  
pp. 1009-1016 ◽  
Author(s):  
Atsunori Nakao ◽  
Gaetano Faleo ◽  
Hiroko Shimizu ◽  
Kiichi Nakahira ◽  
Junichi Kohmoto ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Cytochrome P450 ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ex Vivo ◽  
Ischemia Reperfusion

scholarly journals Dexmedetomidine Attenuates Lung Ischemia-reperfusion Injury in Rats by Reducing Mitochondrial Dysfunction

2020 ◽  
Author(s):  
Yan Zhang ◽  
Yao Lu ◽  
Kai Wang ◽  
Mei-yan Zhou ◽  
Cong-you Wu ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Reperfusion Injury ◽  
Mitochondrial Biogenesis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Weight Ratio ◽  
Oxygenation Index ◽  
Lung Damage ◽  
Peroxisome Proliferator ◽  
Sprague Dawley

Abstract Background: Lung ischemia-reperfusion injury (LIRI) is a significant clinical problem occurring after lung transplantation. LIRI is mediated by the overproduction of reactive oxygen species (ROS) and inflammatory activation. Previous studies have confirmed that dexmedetomidine (DEX) exerts a protective effect on LIRI, which potentially causes severe mitochondrial dysfunction. However, the specific mechanisms remain unclear. Our study was to explore whether dexmedetomidine exerts a beneficial effect on LIRI by reducing mitochondrial dysfunction. Methods: Two different models were used in our study. For the in vivo experiment, thirty-two male Sprague-Dawley rats were randomly divided into Sham, ischemia-reperfusion (I/R), DEX+I/R and DEX+yohimbine+I/R (DY+I/R) groups. Similarly, pulmonary vascular endothelial cells (PVECs) from SD rats were divided into Control, oxygen glucose deprivation (OGD), D+OGD and DY+OGD groups.Results: In our experiment, we confirmed severe lung damage after LIRI that was characterized by significantly pulmonary histopathology injury, a decrease in the oxygenation index (PaO2/FiO2) and an increase in the wet-to-dry weight ratio, while DEX treatment mitigated this damage. In addition, the DEX pretreatment significantly attenuated I/R-induced oxidative stress by decreasing the level of ROS in the mitochondria in vitro. Moreover, the DEX treatment enhanced mitochondrial biogenesis and autophagy by increasing the expression of peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α), mitochondrial transcription factor A (Tfam), PTEN-induced putative kinase 1 (PINK1), Parkin and dynamin 1-like protein 1 (Drp1). Conclusions: These data suggest that DEX may alleviate LIRI by reducing mitochondrial dysfunction through the induction of mitochondrial biogenesis and autophagy.

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