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https://www.readbyqxmd.com/read/28883688/a-controversial-medicolegal-issue-timing-the-onset-of-perinatal-hypoxic-ischemic-brain-injury
#1
REVIEW
Vittorio Fineschi, Rocco Valerio Viola, Raffaele La Russa, Alessandro Santurro, Paola Frati
Perinatal hypoxic-ischemic brain injury, as a result of chronic, subacute, and acute insults, represents the pathological consequence of fetal distress and birth or perinatal asphyxia, that is, "nonreassuring fetal status." Hypoxic-ischemic injury (HII) is typically characterized by an early phase of damage, followed by a delayed inflammatory local response, in an apoptosis-necrosis continuum. In the early phase, the cytotoxic edema and eventual acute lysis take place; with reperfusion, additional damage should be assigned to excitotoxicity and oxidative stress...
2017: Mediators of Inflammation
https://www.readbyqxmd.com/read/28876386/a-possible-relationship-between-gluconeogenesis-and-glycogen-metabolism-in-rabbits-during-myocardial-ischemia
#2
Raquel R DE Aguiar, Daniela F Vale, Renato M DA Silva, Yolanda P Muniz, Fernanda Antunes, Carlos Logullo, André L A Oliveira, Adriana J DE Almeida
Ischemia is responsible for many metabolic abnormalities in the heart, causing changes in organ function. One of modifications occurring in the ischemic cell is changing from aerobic to anaerobic metabolism. This change causes the predominance of the use of carbohydrates as an energy substrate instead of lipids. In this case, the glycogen is essential to the maintenance of heart energy intake, being an important reserve to resist the stress caused by hypoxia, using glycolysis and lactic acid fermentation. In order to study the glucose anaerobic pathways utilization and understand the metabolic adaptations, New Zealand white rabbits were subjected to ischemia caused by Inflow occlusion technique...
August 31, 2017: Anais da Academia Brasileira de Ciências
https://www.readbyqxmd.com/read/28865712/microrna-31-promotes-adverse-cardiac-remodeling-and-dysfunction-in-ischemic-heart-disease
#3
Eliana C Martinez, Shera Lilyanna, Peipei Wang, Leah A Vardy, Xiaofei Jiang, Arunmozhiarasi Armugam, Kandiah Jeyaseelan, Arthur Mark Richards
RATIONALE: Myocardial infarction (MI) triggers a dynamic microRNA response with the potential of yielding therapeutic targets. OBJECTIVE: We aimed to identify novel aberrantly expressed cardiac microRNAs post-MI with potential roles in adverse remodeling in a rat model, and to provide post-ischemic therapeutic inhibition of a candidate pathological microRNA in vivo. METHODS AND RESULTS: Following microRNA array profiling in rat hearts 2 and 14days post-MI, we identified a time-dependent up-regulation of miR-31 compared to sham-operated rats...
September 1, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28852062/farnesoid-x-receptor-activation-protects-the-kidney-from-ischemia-reperfusion-damage
#4
Zhibo Gai, Lei Chu, Zhenqiang Xu, Xiaoming Song, Dongfeng Sun, Gerd A Kullak-Ublick
Farnesoid X receptor (FXR) activation has been reported to reduce inflammation and oxidative stress. Because both inflammation and oxidative stress are critical for tissue destruction during kidney ischemia reperfusion (I/R) injury, we investigated the protective role of FXR against kidney damage induced by I/R in mice. Mice undergoing renal I/R developed the typical features of acute kidney injury (AKI): increased creatinine, albuminuria, tubular necrosis and apoptosis. Inflammatory cytokine production and oxidative stress were also markedly increased...
August 29, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28851980/hypoxic-stress-decreases-c-myc-protein-stability-in-cardiac-progenitor-cells-inducing-quiescence-and-compromising-their-proliferative-and-vasculogenic-potential
#5
Michael A Bellio, Mariana T Pinto, Victoria Florea, Paola A Barrios, Christy N Taylor, Ariel B Brown, Courtney Lamondin, Joshua M Hare, Ivonne H Schulman, Claudia O Rodrigues
Cardiac progenitor cells (CPCs) have been shown to promote cardiac regeneration and improve heart function. However, evidence suggests that their regenerative capacity may be limited in conditions of severe hypoxia. Elucidating the mechanisms involved in CPC protection against hypoxic stress is essential to maximize their cardioprotective and therapeutic potential. We investigated the effects of hypoxic stress on CPCs and found significant reduction in proliferation and impairment of vasculogenesis, which were associated with induction of quiescence, as indicated by accumulation of cells in the G0-phase of the cell cycle and growth recovery when cells were returned to normoxia...
August 29, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28838842/ellagic-acid-antagonizes-bnip3-mediated-mitochondrial-injury-and-necrotic-cell-death-of-cardiac-myocytes
#6
Abhinav Dhingra, Rahul Jayas, Pegah Afshar, Matthew Guberman, Graham Maddaford, Johnathan Gerstein, Brooke Lieberman, Hilary Nepon, Victoria Margulets, Rimpy Dhingra, Lorrie A Kirshenbaum
The Bcl-2 protein Bnip3 is crucial for provoking oxidative injury to mitochondria following anthracycline treatment or ischemia-reperfusion injury. Herein, we investigate the effects of the polyphenolic compound ellagic acid (EA) on Bnip3 mediated mitochondrial injury and necrotic cell death in cardiac myocytes. In contrast to vehicle treated cardiomyocytes, Bnip3 was highly enriched in mitochondrial fractions of cardiac myocytes treated with the anthracycline doxorubicin or in cells subjected to hypoxia (HPX)...
August 25, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28827077/high-potential-defense-mechanisms-of-neocortex-in-a-rat-model-of-transient-asphyxia-induced-cardiac-arrest
#7
Gerburg Keilhoff, Torben Esser, Maximilian Titze, Uwe Ebmeyer, Lorenz Schild
Cardiac arrest (CA) is a common cause of disability and mortality and thus an important risk for human health. Circulatory failure has dramatic consequences for the brain as one of the most oxygen-consuming organs. Hippocampus, striatum and neocortex rate among the most vulnerable brain regions. The neocortex is less sensitive to hypoxia/reperfusion in comparison with the hippocampal CA1 region. That implicates the existence of efficient defense mechanisms in the neocortex against hypoxia/reperfusion injury, which we analyzed in a well-established CA rat model...
August 18, 2017: Brain Research
https://www.readbyqxmd.com/read/28821450/carvedilol-abrogates-hypoxia-induced-oxidative-stress-and-neuroinflammation-in-microglial-bv2-cells
#8
Xiujuan Gao, Bin Wu, Zhijian Fu, Zongwang Zhang, Guangjun Xu
Microglia initially undergo rapid activation in response to injury and stressful stimuli, such as hypoxia. Oxidative stress and the inflammatory response play critical roles in hypoxic-ischemic brain injury. Carvedilol is a β-blocker used to treat high blood pressure and heart failure. In this study, we investigated whether carvedilol had a protective effect against hypoxia-induced oxidative stress and inflammation in microglial BV2 cells. Our results indicate that hypoxic exposure significantly reduced mean cell viability of BV2 microglia, which was significantly restored by carvedilol (10 and 50μM)...
August 15, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28803066/a-novel-ripk1-inhibitor-that-prevents-retinal-degeneration-in-a-rat-glaucoma-model
#9
Yun-Ju Do, Jee-Won Sul, Ki-Hong Jang, Nam Sook Kang, Young-Hoon Kim, Young-Gwan Kim, Eunhee Kim
In glaucoma, retinal ganglion cells (RGCs) are exposed to ischemic stress with elevation of the intraocular pressure and are subsequently lost. Necroptosis, a type of regulated necrosis, is known to play a pivotal role in this loss. We observed that receptor-interacting protein kinase 1 (RIPK1), the key player of necroptosis, was activated by diverse ischemic stresses, including TCZ, chemical hypoxia (CH), and oxygen glucose deprivation (OGD). In this study, we introduce a RIPK1-inhibitory compound (RIC) with a novel scaffold...
August 9, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28765969/ampk-activation-restores-ischemic-post%C3%A2-conditioning-cardioprotection-in-stz%C3%A2-induced-type-1-diabetic-rats-role-of-autophagy
#10
Bin Zhou, Yan Leng, Shao-Qing Lei, Zhong-Yuan Xia
Although the mechanism remains unclear, ischemic post‑conditioning (IPO) is a promising approach to combat myocardial ischemia reperfusion (IR) injury; however, it has been proven ineffective in diabetes. The present study aimed to identify whether hyperglycemia‑induced AMP‑activated protein kinase (AMPK) inhibition contributes to the ineffectiveness of IPO via autophagy attenuation in diabetic hearts. Diabetic and non‑diabetic rats were subjected to myocardial IR and/or IPO with/without treatment with the AMPK activator A‑769662 and/or autophagy inhibitor 3‑methyladenine (3‑MA)...
September 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28762914/-adaptation-to-intermittent-hypoxia-hyperoxia-in-the-rehabilitation-of-patients-with-ischemic-heart-disease-exercise-tolerance-and-quality-of-life
#11
A L Syrkin, O S Glazachev, F Y Kopylov, E N Dudnik, E E Zagaynaya, D S Tuter
AIM: to assess effect of interval hypoxic-hyperoxic training (IT) on exercise tolerance and quality of life of patients with ischemic heart disease (IHD) receiving optimal medical therapy, as well as the safety of IHHT use. METHODS: Patients with stable IHD with functional class II and III angina (n=46) were randomized into two groups: IHHT (n=27, 15 treatments in 3 weeks), and IHHT imitation (n=19). Cardiopulmonary stress test was performed to evaluate the following parameters of exercise tolerance: peak oxygen consumption (VO2peak, VO2peak/kg), % of predicted peak oxygen consumption (%VO2 peak) and anaerobic threshold (VO2AT)...
May 2017: Kardiologiia
https://www.readbyqxmd.com/read/28735240/therapeutic-effects-of-l-cysteine-in-newborn-mice-subjected-to-hypoxia-ischemia-brain-injury-via-the-cbs-h2s-system-role-of-oxidative-stress-and-endoplasmic-reticulum-stress
#12
Song Liu, Danqing Xin, Lingxiao Wang, Tiantian Zhang, Xuemei Bai, Tong Li, Yunkai Xie, Hao Xue, Shishi Bo, Dexiang Liu, Zhen Wang
Neonatal hypoxic-ischemic (HI) injury is a major cause of neonatal death and neurological dysfunction. H2S has been shown to protect against hypoxia-induced injury and apoptosis of neurons. L-Cysteine is catalyzed by cystathionine-β-synthase (CBS) in the brain and sequentially produces endogenous H2S. The present study was designed to investigate whether L-Cysteine could attenuate the acute brain injury and improve neurobehavioral outcomes following HI brain injury in neonatal mice by releasing endogenous H2S...
July 14, 2017: Redox Biology
https://www.readbyqxmd.com/read/28714516/-epigallocatechin-3-gallate-attenuates-myocardial-injury-induced-by-ischemia-reperfusion-in-diabetic-rats-and-in-h9c2-cells-under-hyperglycemic-conditions
#13
Yang Wu, Zhong-Yuan Xia, Bo Zhao, Yan Leng, Juan Dou, Qing-Tao Meng, Shao-Qing Lei, Zhi-Ze Chen, Jie Zhu
(-)-Epigallocatechin gallate (EGCG) exerts multiple beneficial effects on cardiovascular performance. In this study, we aimed to examine the effects of EGCG on diabetic cardiomyopathy during myocardial ischemia/reperfusion (I/R) injury. EGCG (100 mg/kg/day) was administered at week 6 for 2 weeks to diabetic rats following the induction of type 1 diabetes by streptozotocin (STZ). At the end of week 8, the animals were subjected to myocardial I/R injury. The EGCG-elicited structural and functional effects were analyzed...
August 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/28698612/eif2%C3%AE-signaling-regulates-ischemic-osteonecrosis-through-endoplasmic-reticulum-stress
#14
Daquan Liu, Yunlong Zhang, Xinle Li, Jie Li, Shuang Yang, Xiaoxue Xing, Guanwei Fan, Hiroki Yokota, Ping Zhang
Osteonecrosis of the femoral head (ONFH) primarily results from ischemia/hypoxia to the femoral head, and one of the cellular manifestations is the endoplasmic reticulum (ER) stress. To understand possible linkage of ischemic osteonecrosis to the ER stress, a surgery-induced animal model was employed and salubrinal was administered to evaluate the role of ER stress. Salubrinal is a synthetic chemical that inhibits de-phosphorylation of eIF2α, and it can suppress cell death from the ER stress at a proper dose...
July 11, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28698499/molecular-mechanisms-behind-free-radical-scavengers-function-against-oxidative-stress
#15
REVIEW
Fereshteh Ahmadinejad, Simon Geir Møller, Morteza Hashemzadeh-Chaleshtori, Gholamreza Bidkhori, Mohammad-Saeid Jami
Accumulating evidence shows that oxidative stress is involved in a wide variety of human diseases: rheumatoid arthritis, Alzheimer's disease, Parkinson's disease, cancers, etc. Here, we discuss the significance of oxidative conditions in different disease, with the focus on neurodegenerative disease including Parkinson's disease, which is mainly caused by oxidative stress. Reactive oxygen and nitrogen species (ROS and RNS, respectively), collectively known as RONS, are produced by cellular enzymes such as myeloperoxidase, NADPH-oxidase (nicotinamide adenine dinucleotide phosphate-oxidase) and nitric oxide synthase (NOS)...
July 10, 2017: Antioxidants (Basel, Switzerland)
https://www.readbyqxmd.com/read/28657795/p38-mapk-inhibition-improves-heart-function-in-pressure-loaded-right-ventricular-hypertrophy
#16
Baktybek Kojonazarov, Tatyana Novoyatleva, Mario Boehm, Chris Happe, Zaneta Sibinska, Xia Tian, Amna Sajjad, Himal Luitel, Guido Posern, Steven M Evans, Friedrich Grimminger, Hossein A Ghofrani, Norbert Weissmann, Harm J Bogaard, Werner Seeger, Ralph T Schermuly
While p38 MAPK is known to have a role in ischemic heart disease and many other diseases, its contribution to the pathobiology of right ventricular (RV) hypertrophy and failure is unclear. Therefore, we sought to investigate the role of p38 MAPK to the pathophysiology of pressure overload-induced RV hypertrophy and failure. Measurements and Main Results The effects of the p38 MAPK inhibitor PH797804 were investigated in mice with RV hypertrophy/failure caused by exposure to hypoxia or pulmonary artery banding (PAB); in addition, the effects of p38 MAPK inhibition or depletion (by small interfering RNA) were studied in isolated mouse RV fibroblasts...
June 28, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28656194/excessive-nnos-no-ampk-signaling-activation-mediated-by-the-blockage-of-the-cbs-h2s-system-contributes-to-oxygen%C3%A2-glucose-deprivation%C3%A2-induced-endoplasmic-reticulum-stress-in-pc12%C3%A2-cells
#17
Rui Zhang, Yong-Quan Lin, Wei-Sheng Wang, Xin-Qiang Wang
Hypoxic‑ischemia stress causes severe brain injury, leading to death and disability worldwide. Although it has been reported that endoplasmic reticulum (ER) stress is an essential step in the progression of hypoxia or ischemia‑induced brain injury, the underlying molecular mechanisms are and have not yet been fully elucidated. Accumulating evidence has indicated that both nitric oxide (NO) and hydrogen sulfide (H2S) play an important role in the development of cerebral ischemic injury. In the present study, we aimed to investigate the effect of the association between NO signaling and the cystathionine β‑synthase (CBS)/H2S system on ER stress in a cell model of cerebral hypoxia‑ischemia injury...
June 21, 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/28634450/leonurine-improves-age-dependent-impaired-angiogenesis-possible-involvement-of-mitochondrial-function-and-hif-1%C3%AE-dependent-vegf-activation
#18
Jia Qi, Jing J Wang, Jun L Duan, Zhao Y Lu, Yang G Yuan
Objective: Advanced age is associated with impaired angiogenesis in part because of mitochondrial dysfunction. We have recently reported that leonurine exerts protective effects in neuron via regulation of mitochondrial function. The aim of this study was to explore whether leonurine is able to attenuate mitochondrial dysfunction and to enhance angiogenesis in old rats with hindlimb ischemia. Methods and Results: At day 14 after surgery, hypoxia-inducible factor (HIF)-1α and vascular endothelial growth factor (VEGF) expression was decreased in the ischemic muscle of aged animals, which was accompanied by enhanced oxidative stress, increased mitochondrial damage, decreased capillary density, and reduced limb perfusion compared with young mice...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28629519/erythropoietin-endogenous-protection-of-ischemic-brain
#19
Robert T Mallet, Myoung-Gwi Ryou
The human brain requires uninterrupted delivery of blood-borne oxygen and nutrients to sustain its function. Focal ischemia, particularly, ischemic stroke, and global ischemia imposed by cardiac arrest disrupt the brain's fuel supply. The resultant ATP depletion initiates a complex injury cascade encompassing intracellular Ca(2+) overload, glutamate excitotoxicity, oxido-nitrosative stress, extracellular matrix degradation, and inflammation, culminating in neuronal and astroglial necrosis and apoptosis, neurocognitive deficits, and even death...
2017: Vitamins and Hormones
https://www.readbyqxmd.com/read/28625734/synthesis-and-cardiomyocyte-protection-activity-of-crocetin-diamide-derivatives
#20
Jin Gao, Ming Chen, Xue-Cong Ren, Xiao-Bo Zhou, Qiang Shang, Wen-Qi Lu, Pei Luo, Zhi-Hong Jiang
A series of novel diamide derivatives (2-8) of crocetin (1) were synthesized and evaluated for their cardioprotective activity in vitro. Using well-established model of hypoxia-induced injury in H9c2 cells, we investigated the effects of 9 compounds and positive drug nicorandil on cellular cytotoxicity by MTT assay, mitochondrial viable staining, LDH activity and mitochondrial membrane potential (MMP). Among the new derivatives, compounds 3 and 4 with good liposolubility showed significantly potent activity than crocetin (1) against hypoxia-induced cytotoxicity...
June 15, 2017: Fitoterapia
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