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Reperfusion injury

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https://www.readbyqxmd.com/read/27936461/pterostilbene-protects-against-myocardial-ischemia-reperfusion-injury-via-suppressing-oxidative-nitrative-stress-and-inflammatory-response
#1
Zhaoxia Yu, Shaohua Wang, Xiangyang Zhang, Ying Li, Qiang Zhao, Tao Liu
Recent studies have shown that pterostilbene (Pte) confers protection against myocardial ischemia/reperfusion injury. The oxidative/nitrative stress and inflammation induce injury after myocardial ischemia/reperfusion. The present study was designed to evaluate whether treatment with Pte attenuates oxidative/nitrative stress and inflammation in myocardial ischemia/reperfusion (MI/R). Rats were subjected to 30min of myocardial ischemia and 3h of reperfusion, and the rats were administered with vehicle or Pte...
December 6, 2016: International Immunopharmacology
https://www.readbyqxmd.com/read/27936094/lutein-attenuates-both-apoptosis-and-autophagy-upon-cobalt-ii-chloride-induced-hypoxia-in-rat-m%C3%A5-ller-cells
#2
Frederic K C Fung, Betty Y K Law, Amy C Y Lo
Retinal ischemia/reperfusion injury is a common feature of various retinal diseases such as glaucoma and diabetic retinopathy. Lutein, a potent anti-oxidant, is used to improve visual function in patients with age-related macular degeneration (AMD). Lutein attenuates apoptosis, oxidative stress and inflammation in animal models of acute retinal ischemia/hypoxia. Here, we further show that lutein improved Műller cell viability and enhanced cell survival upon hypoxia-induced cell death through regulation of intrinsic apoptotic pathway...
2016: PloS One
https://www.readbyqxmd.com/read/27936014/inhibition-of-interleukin-6-receptor-in-a-murine-model-of-myocardial-ischemia-reperfusion
#3
Minke H T Hartman, Inge Vreeswijk-Baudoin, Hilde E Groot, Kees W A van de Kolk, Rudolf A de Boer, Irene Mateo Leach, Rozemarijn Vliegenthart, Herman H W Sillje, Pim van der Harst
BACKGROUND: Interleukin-6 (IL-6) levels are upregulated in myocardial infarction. Recent data suggest a causal role of the IL-6 receptor (IL-6R) in coronary heart disease. We evaluated if IL-6R blockade by a monoclonal antibody (MR16-1) prevents the heart from adverse left ventricular remodeling in a mouse model of ischemia-reperfusion (I/R). METHODS: CJ57/BL6 mice underwent I/R injury (left coronary artery ligation for 45 minutes) or sham surgery, and thereafter received MR16-1 (2mg/mouse) 5 minutes before reperfusion and 0...
2016: PloS One
https://www.readbyqxmd.com/read/27933431/effect-of-remote-ischaemic-preconditioning-on-liver-injury-in-patients-undergoing-major-hepatectomy-for-colorectal-liver-metastasis-a-pilot-randomised-controlled-feasibility-trial
#4
Sanjeev Kanoria, Francis P Robertson, Naimish N Mehta, Giuseppe Fusai, Dinesh Sharma, Brian R Davidson
BACKGROUND: Liver resection produces excellent long-term survival for patients with colorectal liver metastases but is associated with significant morbidity and mortality from ischaemia reperfusion injury (IRI). Remote ischaemic preconditioning (RIPC) can reduce the effect of IRI. This pilot randomised controlled trial evaluated RIPC in patients undergoing major hepatectomy at the Royal Free Hospital, London. METHODS: Sixteen patients were randomised to RIPC or sham control...
December 8, 2016: World Journal of Surgery
https://www.readbyqxmd.com/read/27933093/long-term-consumption-of-an-obesogenic-high-fat-diet-prior-to-ischemia-reperfusion-mediates-cardioprotection-via-epac1-dependent-signaling
#5
F Edland, A Wergeland, R Kopperud, K S Åsrud, E A Hoivik, S L Witsø, R Æsøy, L Madsen, K Kristiansen, M Bakke, S O Døskeland, A K Jonassen
BACKGROUND: Obesity is still considered a risk factor for cardiovascular disease, although more recent knowledge also suggests obesity to be associated with reduced morbidity and mortality - the "obesity paradox". This study explores if long-term feeding of an obesogenic high fat diet renders the myocardium less susceptible to ischemic-reperfusion induced injury via Epac-dependent signaling. METHODS: Wild type (wt), Epac1 (Epac1(-/-)) and Epac2 (Epac2(-/-)) deficient mice were fed a high fat (HFD) or normal chow diet (ND) for 33 ± 1 weeks...
2016: Nutrition & Metabolism
https://www.readbyqxmd.com/read/27932476/high-fat-diet-induced-lysosomal-dysfunction-and-impaired-autophagic-flux-contribute-to-lipotoxicity-in-the-kidney
#6
Takeshi Yamamoto, Yoshitsugu Takabatake, Atsushi Takahashi, Tomonori Kimura, Tomoko Namba, Jun Matsuda, Satoshi Minami, Jun-Ya Kaimori, Isao Matsui, Taiji Matsusaka, Fumio Niimura, Motoko Yanagita, Yoshitaka Isaka
Excessive fat intake contributes to the progression of metabolic diseases via cellular injury and inflammation, a process termed lipotoxicity. Here, we investigated the role of lysosomal dysfunction and impaired autophagic flux in the pathogenesis of lipotoxicity in the kidney. In mice, a high-fat diet (HFD) resulted in an accumulation of phospholipids in enlarged lysosomes within kidney proximal tubular cells (PTCs). In isolated PTCs treated with palmitic acid, autophagic degradation activity progressively stagnated in association with impaired lysosomal acidification and excessive lipid accumulation...
December 8, 2016: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/27932075/non-enzymatic-oxidized-metabolite-of-dha-4-rs-4-f4t-neuroprostane-protects-the-heart-against-reperfusion-injury
#7
Jérôme Roy, Jérémy Fauconnier, Camille Oger, Charlotte Farah, Claire Angebault-Prouteau, Jérôme Thireau, Patrice Bideaux, Valérie Scheuermann, Valérie Bultel-Poncé, Marie Demion, Jean-Marie Galano, Thierry Durand, Jetty Chung-Yung Lee, Jean-Yves Le Guennec
Acute myocardial infarction leads to an increase in oxidative stress and lipid peroxidation. 4(RS)-4-F4t-Neuroprostane (4-F4t-NeuroP) is a mediator produced by non-enzymatic free radical peroxidation of the cardioprotective polyunsaturated fatty acid, docosahexaenoic acid (DHA). In this study, we investigated whether intra-cardiac delivery of 4-F4t-NeuroP (0.03mg/kg) prior to occlusion (ischemia) prevents and protects rat myocardium from reperfusion damages. Using a rat model of ischemic-reperfusion (I/R), we showed that intra-cardiac infusion of 4-F4t-NeuroP significantly decreased infarct size following reperfusion (-27%) and also reduced ventricular arrhythmia score considerably during reperfusion (-41%)...
December 5, 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/27931646/haemodynamic-coherence-in-haemorrhagic-shock
#8
REVIEW
Nicolas Libert, Anatole Harrois, Jacques Duranteau
In case of haemorrhage, a combination of low volume fluid resuscitation and permissive hypotension is used to avoid the adverse effects of early aggressive fluid resuscitation. During this phase, occult microvascular hypoperfusion can possibly develop over time. After controlling the bleeding, it is expected that optimization of macrocirculation will result in an improvement in microcirculation. However, this is the case only without alterations in microcirculation regulation. Haemodynamic coherence must be maintained to expect the restoration of microcirculation through systemic haemodynamic-driven resuscitation...
December 2016: Best Practice & Research. Clinical Anaesthesiology
https://www.readbyqxmd.com/read/27931589/a-new-chemical-compound-necrox-7-acts-as-a-necrosis-modulator-by-inhibiting-high-mobility-group-box-1-protein-release-during-massive-ischemia-reperfusion-injury
#9
J H Lee, K M Park, Y J Lee, J H Kim, S H Kim
BACKGROUND: Necrotic cell death is common in a wide variety of pathologic conditions, including ischemia-reperfusion (IR) injury. The aim of this study was to develop an IR injury-induced hepatic necrosis model in dogs by means of selective left hepatic inflow occlusion and to test the efficacy of a new chemical compound, NecroX-7, against the IR injury-induced hepatic damage. METHODS: A group of male Beagle dogs received intravenous infusions of either vehicle or different doses of NecroX-7 (1...
December 2016: Transplantation Proceedings
https://www.readbyqxmd.com/read/27931559/role-of-cardiac-renin-angiotensin-system-in-ischemia-reperfusion-injury-and-preconditioning-of-heart
#10
REVIEW
Vimal Agrawal, Jeetendra Kumar Gupta, Shaiba Sana Qureshi, Vishal Kumar Vishwakarma
Cardio-vascular diseases are the leading cause of morbidity and mortality. Ischemia is a state of oxygen deprivation in tissues, whereas reperfusion is restoration of blood flow in ischemic tissues. Myocardial damage of tissue during reperfusion after ischemic insult is known as myocardial ischemia-reperfusion (I/R) injury. It induces damage to cardiac muscle via increasing expression of oxygen, sodium and calcium ions which are responsible in the activation of proteases and cell death. Heart renin angiotensin system (RAS) plays an important role in the myocardial ischemia and reperfusion injury...
November 2016: Indian Heart Journal
https://www.readbyqxmd.com/read/27931079/protecting-the-mitochondria-against-ischemia-reperfusion-a-gassy-solution
#11
EDITORIAL
Thierry Hauet, Raphael Thuillier
Organ transplantation success has seen great improvements in past decades due to progresses in immune-suppressive regiments. However, lack of long-term graft outcome improvement, added to increased marginal donors use, has recently shifted the focus towards the peri-transplant period and particularly ischemia reperfusion injury (IRI). The recent acknowledgment of the link between IRI and outcome, short or long term, has rekindled interest in the study of the physiopathology associated with organ preservation and the methods to optimize it...
December 8, 2016: American Journal of Transplantation
https://www.readbyqxmd.com/read/27930802/ap39-a-mitochondria-targeting-hydrogen-sulfide-h2-s-donor-protects-against-myocardial-reperfusion-injury-independently-of-salvage-kinase-signalling
#12
Qutuba G Karwi, Julia Bornbaum, Kerstin Boengler, Roberta Torregrossa, Matthew Whiteman, Mark E Wood, Rainer Schulz, Gary F Baxter
BACKGROUND AND PURPOSE: H2 S protects myocardium against ischaemia-reperfusion injury. This protection may involve the cytosolic reperfusion injury salvage kinase (RISK) pathway, but direct effects on mitochondrial function are possible. Here, we investigated the potential cardioprotective effect of mitochondria-specific H2 S donor, AP39, at reperfusion against ischaemia/reperfusion injury. EXPERIMENTAL APPROACH: Anaesthetised rats underwent myocardial (30 min ischaemia/120 min reperfusion) with randomisation to receive interventions prior to reperfusion: vehicle, AP39 (0...
December 8, 2016: British Journal of Pharmacology
https://www.readbyqxmd.com/read/27930699/estrogen-protects-the-female-heart-from-ischemia-reperfusion-injury-through-manganese-superoxide-dismutase-phosphorylation-by-mitochondrial-p38%C3%AE-at-threonine-79-and-serine-106
#13
Tao Luo, Han Liu, Jin Kyung Kim
A collective body of evidence indicates that estrogen protects the heart from myocardial ischemia/reperfusion (I/R) injury, but the underlying mechanism remains incompletely understood. We have previously delineated a novel mechanism of how 17β-estradiol (E2) protects cultured neonatal rat cardiomyocytes from hypoxia/reoxygenation (H/R) by identifying a functionally active mitochondrial pool of p38β and E2-driven upregulation of manganese superoxide dismutase (MnSOD) activity via p38β, leading to the suppression of reactive oxygen species (ROS) and apoptosis...
2016: PloS One
https://www.readbyqxmd.com/read/27930351/hydrogen-peroxide-responsive-nanoparticle-reduces-myocardial-ischemia-reperfusion-injury
#14
Soochan Bae, Minhyung Park, Changsun Kang, Serkan Dilmen, Tae Hi Kang, Dong Goo Kang, Qingen Ke, Seung Uk Lee, Dongwon Lee, Peter M Kang
BACKGROUND: During myocardial ischemia/reperfusion (I/R), a large amount of reactive oxygen species (ROS) is produced. In particular, overproduction of hydrogen peroxide (H2O2) is considered to be a main cause of I/R-mediated tissue damage. We generated novel H2O2-responsive antioxidant polymer nanoparticles (PVAX and HPOX) that are able to target the site of ROS overproduction and attenuate the oxidative stress-associated diseases. In this study, nanoparticles were examined for their therapeutic effect on myocardial I/R injury...
November 14, 2016: Journal of the American Heart Association
https://www.readbyqxmd.com/read/27929536/hyperhomocysteinemia-causes-er-stress-and-impaired-autophagy-that-is-reversed-by-vitamin-b-supplementation
#15
Madhulika Tripathi, Cheng Wu Zhang, Brijesh Kumar Singh, Rohit Anthony Sinha, Kyaw Thu Moe, Deidre Anne DeSilva, Paul Michael Yen
Hyperhomocysteinemia (HHcy) is a well-known risk factor for stroke; however, its underlying molecular mechanism remains unclear. Using both mouse and cell culture models, we have provided evidence that impairment of autophagy has a central role in HHcy-induced cellular injury in the mouse brain. We observed accumulation of LC3B-II and p62 that was associated with increased MTOR signaling in human and mouse primary astrocyte cell cultures as well as a diet-induced mouse model of HHcy, HHcy decreased lysosomal membrane protein LAMP2, vacuolar ATPase (ATP6V0A2), and protease cathepsin D, suggesting that lysosomal dysfunction also contributed to the autophagic defect...
December 8, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27929137/inhibition-of-pkr-protects-against-h2o2-induced-injury-on-neonatal-cardiac-myocytes-by-attenuating-apoptosis-and-inflammation
#16
Yongyi Wang, Min Men, Bo Xie, Jianggui Shan, Chengxi Wang, Jidong Liu, Hui Zheng, Wengang Yang, Song Xue, Changfa Guo
Reactive oxygenation species (ROS) generated from reperfusion results in cardiac injury through apoptosis and inflammation, while PKR has the ability to promote apoptosis and inflammation. The aim of the study was to investigate whether PKR is involved in hydrogen peroxide (H2O2) induced neonatal cardiac myocytes (NCM) injury. In our study, NCM, when exposed to H2O2, resulted in persistent activation of PKR due to NCM endogenous RNA. Inhibition of PKR by 2-aminopurine (2-AP) or siRNA protected against H2O2 induced apoptosis and injury...
December 8, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27928652/enhanced-proteostasis-in-post-ischemic-stroke-mouse-brains-by-ubiquilin-1-promotes-functional-recovery
#17
Yanying Liu, Fangfang Qiao, Hongmin Wang
Stroke is pathologically associated with oxidative stress, protein damage, and neuronal loss. We previously reported that overexpression of a ubiquitin-like protein, ubiquilin-1 (Ubqln), protects neurons against ischemia-caused brain injury, while knockout of the gene exacerbates cerebral ischemia-caused neuronal damage and delays functional recovery. Although these observations indicate that Ubqln is a potential therapeutic target, transgenic manipulation-caused overexpression of Ubqln occurs before the event of ischemic stroke, and it remains unknown whether delayed Ubqln overexpression in post-ischemic brains within a clinically relevant time frame is still beneficial...
December 7, 2016: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/27928644/cardioprotection-by-remote-ischemic-conditioning-and-its-signal-transduction
#18
REVIEW
Petra Kleinbongard, Andreas Skyschally, Gerd Heusch
Cardioprotective strategies aim to salvage myocardium from ischemia/reperfusion injury and to reduce infarct size and its consequences. Different stimuli, acting at sites remote from the heart (remote conditioning), activate molecular self-defense mechanisms at the target organ heart as well as in other parenchymal organs. Remote conditioning of the heart has been established in many experimental studies and successfully translated to patients. Remote ischemic conditioning by short repetitive cycles of ischemia/reperfusion on an extremity reduces infarct size and improves the prognosis of patients with reperfused myocardial infarction...
December 7, 2016: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/27928159/effect-of-trem-1-blockade-and-single-nucleotide-variants-in-experimental-renal-injury-and-kidney-transplantation
#19
A Tammaro, J Kers, D Emal, I Stroo, G J D Teske, L M Butter, N Claessen, J Damman, M Derive, G Navis, S Florquin, J C Leemans, M C Dessing
Renal ischemia reperfusion (IR)-injury induces activation of innate immune response which sustains renal injury and contributes to the development of delayed graft function (DGF). Triggering receptor expressed on myeloid cells-1 (TREM-1) is a pro-inflammatory evolutionary conserved pattern recognition receptor expressed on a variety of innate immune cells. TREM-1 expression increases following acute and chronic renal injury. However, the function of TREM-1 in renal IR is still unclear. Here, we investigated expression and function of TREM-1 in a murine model of renal IR using different TREM-1 inhibitors: LP17, LR12 and TREM-1 fusion protein...
December 8, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27927779/depletion-of-gut-microbiota-protects-against-renal-ischemia-reperfusion-injury
#20
Diba Emal, Elena Rampanelli, Ingrid Stroo, Loes M Butter, Gwendoline J Teske, Nike Claessen, Geurt Stokman, Sandrine Florquin, Jaklien C Leemans, Mark C Dessing
An accumulating body of evidence shows that gut microbiota fulfill an important role in health and disease by modulating local and systemic immunity. The importance of the microbiome in the development of kidney disease, however, is largely unknown. To study this concept, we depleted gut microbiota with broad-spectrum antibiotics and performed renal ischemia-reperfusion (I/R) injury in mice. Depletion of the microbiota significantly attenuated renal damage, dysfunction, and remote organ injury and maintained tubular integrity after renal I/R injury...
December 7, 2016: Journal of the American Society of Nephrology: JASN
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