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Hypoxia-ischemia

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https://www.readbyqxmd.com/read/28930963/role-of-autophagy-and-its-molecular-mechanisms-in-mice-intestinal-tract-after-severe-burn
#1
Duan Y Zhang, Wei Qiu, PeiS Jin, Peng Wang, Yong Sun
BACKGROUND: Severe burn can lead to hypoxia/ischemia of intestinal mucosa. Autophagy is the process of intracellular degradation, which is essential for cell survival under stresses, such as hypoxia/ischemia and nutrient deprivation. The present study was designed to investigate whether there were changes in intestinal autophagy after severe burn in mice and further to explore the effect and molecular mechanisms of autophagy on intestinal injury. METHODS: This study includes three experiments...
October 2017: Journal of Trauma and Acute Care Surgery
https://www.readbyqxmd.com/read/28928282/dnmt1-dependent-chk1-pathway-suppression-is-protective-against-neuron-division
#2
Mio Oshikawa, Kei Okada, Hidenori Tabata, Koh-Ichi Nagata, Itsuki Ajioka
Neuronal differentiation and cell-cycle exit are tightly coordinated, even in pathological situations. When pathological neurons re-enter the cell cycle and progress through the S phase, they undergo cell death instead of division. However, the mechanisms underlying mitotic resistance are mostly unknown. Here, we have found that acute inactivation of retinoblastoma (Rb) family proteins (Rb, p107 and p130) in mouse postmitotic neurons leads to cell death after S-phase progression. Checkpoint kinase 1 (Chk1) pathway activation during the S phase prevented the cell death, and allowed the division of cortical neurons that had undergone acute Rb family inactivation, oxygen-glucose deprivation (OGD) or in vivo hypoxia-ischemia...
September 15, 2017: Development
https://www.readbyqxmd.com/read/28901374/ferulic-acid-exerts-neuroprotective-effects-against-cerebral-ischemia-reperfusion-induced-injury-via-antioxidant-and-anti-apoptotic-mechanisms-in%C3%A2-vitro-and-in%C3%A2-vivo
#3
Zhongkun Ren, Rongping Zhang, Yuanyuan Li, Yu Li, Zhiyong Yang, Hui Yang
Ferulic acid (FA) is a derivative of cinnamic acid. It is used in the treatment of heart head blood-vessel disease and exerts protective effects against hypoxia/ischemia-induced cell injury in the brain. This study investigated the potential neuroprotective effects of FA against ischemia/reperfusion (I/R)-induced brain injury in vivo and in vitro through hematoxylin and eosin (H&E) and Nissl staining assays, flow cytometry, Hoechst 33258 staining, quantitative PCR, western blot analysis and fluorescence microscopic analysis...
September 7, 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/28878624/cell-death-in-the-developing-brain-after-hypoxia-ischemia
#4
REVIEW
Claire Thornton, Bryan Leaw, Carina Mallard, Syam Nair, Masako Jinnai, Henrik Hagberg
Perinatal insults such as hypoxia-ischemia induces secondary brain injury. In order to develop the next generation of neuroprotective therapies, we urgently need to understand the underlying molecular mechanisms leading to cell death. The cell death mechanisms have been shown to be quite different in the developing brain compared to that in the adult. The aim of this review is update on what cell death mechanisms that are operating particularly in the setting of the developing CNS. In response to mild stress stimuli a number of compensatory mechanisms will be activated, most often leading to cell survival...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28875429/regional-differences-in-cerebral-glucose-metabolism-after-cardiac-arrest-and-resuscitation-in-rats-using-18-f-fdg-positron-emission-tomography-and-autoradiography
#5
Alessandro Putzu, Silvia Valtorta, Giuseppe Di Grigoli, Matthias Haenggi, Sara Belloli, Antonio Malgaroli, Marco Gemma, Giovanni Landoni, Luigi Beretta, Rosa Maria Moresco
BACKGROUND: Cardiac arrest is an important cause of morbidity and mortality. Brain injury severity and prognosis of cardiac arrest patients are related to the cerebral areas affected. To this aim, we evaluated the variability and the distribution of brain glucose metabolism after cardiac arrest and resuscitation in an adult rat model. METHODS: Ten rats underwent 8-min cardiac arrest, induced with a mixture of potassium and esmolol, and resuscitation, performed with chest compressions and epinephrine...
September 5, 2017: Neurocritical Care
https://www.readbyqxmd.com/read/28854873/effects-and-mechanism-of-dexmedetomidine-on-neuronal-cell-injury-induced-by-hypoxia-ischemia
#6
Ya-Jun Liu, Duan-Yu Wang, Yong-Jian Yang, Wei-Fu Lei
BACKGROUND: The present study aims to investigate the protective effects of dexmedetomidine (DMED) on hypoxia ischemia injury induced by oxygen and glucose deprivation (OGD) in PC12 and primary neuronal cells. METHODS: PC12 cells exposed to OGD was used to establish ischemia model. The OGD-induced cell injury was evaluated by alterations of cell viability, apoptosis and expressions of apoptosis-associated proteins. Oxidative stress and expressions of neurotrophic factors after OGD and DMED treatments were also explored...
August 30, 2017: BMC Anesthesiology
https://www.readbyqxmd.com/read/28843827/ptpn21-protects-pc12-cell-against-oxygen-glucose-deprivation-by-activating-cdk5-through-erk1-2-signaling-pathway
#7
Ningning Cui, Hui Lu, Meng Li, Qiuyue Yan
PTPN21, a cytosolic non-receptor tyrosine phosphatase isolated from human skeletal muscle, was reported to promote neuronal survival. Nevertheless, it is not clear whether PTPN21 plays a role in hypoxia ischemia-induced neuronal injury. A proper understanding of the PTPN21 mechanism in neuron growth regulation is limited. In this study, we investigated the neuroprotective effects and potential mechanism of PTPN21 on oxygen glucose deprivation (OGD)-injured PC12 cells. The ischemic stroke model of PC12 cells was made by OGD for 2h, after transfection of the PTPN21 siRNA and pcDNA 3...
August 24, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28841577/experimental-neonatal-hypoxia-ischemia-causes-long-lasting-changes-of-oxidative-stress-parameters-in-the-hippocampus-and-the-spleen
#8
Felipe Kawa Odorcyk, Janaína Kolling, Eduardo Farias Sanches, Angela T S Wyse, Carlos Alexandre Netto
Neonatal hypoxia ischemia (HI) is the main cause of mortality and morbidity in newborns. The mechanisms involved in its progression start immediately and persist for several days. Oxidative stress and inflammation are determinant factors of the severity of the final lesion. The spleen plays a major part in the inflammatory response to HI. This study assessed the temporal progression of HI-induced alterations in oxidative stress parameters in the hippocampus, the most affected brain structure, and in the spleen...
August 25, 2017: Journal of Perinatal Medicine
https://www.readbyqxmd.com/read/28803128/tetrahydrobiopterin-in-antenatal-brain-hypoxia-ischemia-induced-motor-impairments-and-cerebral-palsy
#9
REVIEW
Jeannette Vasquez-Vivar, Zhongjie Shi, Kehuan Luo, Karthikeyan Thirugnanam, Sidhartha Tan
Antenatal brain hypoxia-ischemia, which occurs in cerebral palsy, is considered a significant cause of motor impairments in children. The mechanisms by which antenatal hypoxia-ischemia causes brain injury and motor deficits still need to be elucidated. Tetrahydrobiopterin is an important enzyme cofactor that is necessary to produce neurotransmitters and to maintain the redox status of the brain. A genetic deficiency of this cofactor from mutations of biosynthetic or recycling enzymes is a well-recognized factor in the development of childhood neurological disorders characterized by motor impairments, developmental delay, and encephalopathy...
August 3, 2017: Redox Biology
https://www.readbyqxmd.com/read/28776186/home-sweet-home-the-neural-stem-cell-niche-throughout-development-and-after-injury
#10
REVIEW
Rebecca M Ruddy, Cindi M Morshead
Neural stem cells and their progeny reside in two distinct neurogenic niches within the mammalian brain: the subventricular zone and the dentate gyrus. The interplay between the neural stem cells and the niche in which they reside can have significant effects on cell kinetics and neurogenesis. A comprehensive understanding of the changes to the niche that occur through postnatal development and aging, as well as following injury, is relevant for developing therapeutics and interventions to promote neural repair...
August 3, 2017: Cell and Tissue Research
https://www.readbyqxmd.com/read/28774372/-expression-rhythm-of-autophagic-gene-in-neurons-of-neonatal-rats-with-hypoxia-ischemia-and-its-regulatory-mechanism
#11
Shi-Ping Li, Jiang-Hu Zhu, Feng-Yan Zhao, Zhen Zheng, De-Zhi Mu, Yi Qu
OBJECTIVE: To investigate the expression of autophagic gene and circadian gene in the neurons of neonatal rats after hypoxic-ischemic brain damage and the mechanism of nerve injury induced by hypoxia/ischemia. METHODS: Twelve Sprague-Dawley (SD) rats were randomly divided into hypoxic-ischemic (HI) group and sham-operation group, with 6 rats in each group. Ligation of the right common carotid artery and hypoxic treatment were performed to establish a model of hypoxic-ischemic brain damage...
August 2017: Zhongguo Dang Dai Er Ke za Zhi, Chinese Journal of Contemporary Pediatrics
https://www.readbyqxmd.com/read/28760642/galantamine-administration-reduces-reactive-astrogliosis-and-upregulates-the-anti-oxidant-enzyme-catalase-in-rats-submitted-to-neonatal-hypoxia-ischemia
#12
F K Odorcyk, F Nicola, L E Duran-Carabali, F Figueiró, J Kolling, A Vizuete, E L Konrath, C A Gonçalves, A T S Wyse, C A Netto
Neonatal hypoxia ischemia (HI) plays a role in the etiology of several neurological pathologies and causes severe sequelae. Acetylcholine is a neurotransmitter in the central nervous system and cholinesterase inhibitors have demonstrated a positive action over HI induced deficits. In order to evaluate the effects of pre and post-hypoxia administrations of galantamine, a cholinesterase inhibitor, in a model of perinatal HI, Wistar rats in the post-natal day 7 (PND7) were subjected to a combination of unilateral occlusion of the right carotid artery with the exposure to a 1h hypoxia...
July 29, 2017: International Journal of Developmental Neuroscience
https://www.readbyqxmd.com/read/28748754/neuroprotection-in-hypoxic-ischemic-brain-injury-targeting-glial-cells
#13
María Inés Herrera, Sofia Mucci, George E Barreto, Rodolfo Kolliker-Frers, Francisco Capani
Brain injury constitutes a disabling health condition of several etiologies. One of the major causes of brain injury is hypoxia-ischemia. Until recently, pharmacological treatments were solely focused on neurons. In the last decades, glial cells started to be considered as alternative targets for neuroprotection. Novel treatments for hypoxia-ischemia intend to modulate reactive forms of glial cells, and/or potentiate their recovery response. In this review, we summarize these neuroprotective strategies in hypoxia-ischemia and discuss their mechanisms of action...
July 27, 2017: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28747873/mitochondria-bioenergetics-and-excitotoxicity-new-therapeutic-targets-in-perinatal-brain-injury
#14
REVIEW
Bryan Leaw, Syam Nair, Rebecca Lim, Claire Thornton, Carina Mallard, Henrik Hagberg
Injury to the fragile immature brain is implicated in the manifestation of long-term neurological disorders, including childhood disability such as cerebral palsy, learning disability and behavioral disorders. Advancements in perinatal practice and improved care mean the majority of infants suffering from perinatal brain injury will survive, with many subtle clinical symptoms going undiagnosed until later in life. Hypoxic-ischemia is the dominant cause of perinatal brain injury, and constitutes a significant socioeconomic burden to both developed and developing countries...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28741035/biomarkers-of-hepatic-injury-and-function-in-neonatal-hypoxic-ischemic-encephalopathy-and-with-therapeutic-hypothermia
#15
Hemananda Muniraman, Danielle Gardner, Jane Skinner, Anna Paweletz, Anitha Vayalakkad, Ying Hui Chee, Clare Clifford, Sunil Sanka, Vidheya Venkatesh, Anna Curley, Suresh Victor, Mark A Turner, Paul Clarke
Therapeutic hypothermia (TH) is now provided as standard care to infants with moderate-severe hypoxic ischemic encephalopathy (HIE). The role of TH in limiting neuronal injury is well recognized, but its effect on hepatic injury which occurs frequently in neonatal HIE is not known. Our objective was to characterize biomarkers of liver injury and function in the setting of neonatal HIE and to describe whether HIE severity and provision of TH influence these hepatic biomarkers. We performed a multicenter retrospective study and compared hepatic biomarkers obtained during the first postnatal week, according to the severity of HIE and whether treated with TH...
July 24, 2017: European Journal of Pediatrics
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
#16
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/28723885/term-versus-preterm-cord-blood-cells-for-the-prevention-of-preterm-brain-injury
#17
Jingang Li, Tamara Yawno, Amy Sutherland, Jan Loose, Ilias Nitsos, Beth J Allison, Robert Bischof, Courtney A McDonald, Graham Jenkin, Suzanne L Miller
BACKGROUND: White matter brain injury in preterm infants can induce neurodevelopmental deficits. Umbilical cord blood (UCB) cells demonstrate neuroprotective properties, but it is unknown whether cells obtained from preterm versus term cord blood have similar efficacy. This study compared the ability of term cord blood (TCB) versus preterm cord blood (PCB) cells to reduce white matter injury in preterm fetal sheep. METHODS: Hypoxia-ischemia (HI) was induced in fetal sheep (0...
July 19, 2017: Pediatric Research
https://www.readbyqxmd.com/read/28721600/resveratrol-ameliorates-hypoxia-ischemia-induced-brain-injury-in-the-neonatal-rat-via-the-mir-96-bax-axis
#18
Hongen Bian, Haijun Shan, Tuanying Chen
OBJECTIVE: This study was aimed to investigate the mechanism of resveratrol on amelioration of hypoxia/ischemia (H/I)-induced brain injury. METHODS: The RT-PCR and western blot were used to detect the mRNA and protein expressions, respectively. The PC12 cell induced by OGD/R was as in vitro H/I brain injury model. The luciferase reporter assay was used to prove the relationship between Bax and miR-96, and the cell apoptosis was detected by MTT assay. The loss of MBP+ area in neonatal rats analyzed by immunohistochemistry was to evaluate the extent of brain injury...
July 18, 2017: Child's Nervous System: ChNS: Official Journal of the International Society for Pediatric Neurosurgery
https://www.readbyqxmd.com/read/28708259/rapid-modulation-of-the-silent-information-regulator-1-by-melatonin-after-hypoxia-ischemia-in-the-neonatal-rat-brain
#19
Silvia Carloni, Giulia Riparini, Giuseppe Buonocore, Walter Balduini
Increasing evidence indicates that melatonin possesses protective effects toward different kinds of damage in various organs, including the brain. In a neonatal model of hypoxia-ischemia (HI), melatonin was neuroprotective and preserved the expression of the silent information regulator 1 (SIRT1) 24 hours after the insult. This study aimed to gain more insight into the role of SIRT1 in the protective effect of melatonin after HI by studying the early (1 hour) modulation of SIRT1 and its downstream targets, and the consequences on necrosis, apoptosis, autophagy, and glial cell activation...
July 14, 2017: Journal of Pineal Research
https://www.readbyqxmd.com/read/28706574/neuronal-damage-induced-by-perinatal-asphyxia-is-attenuated-by-postinjury-glutaredoxin-2-administration
#20
Juan Ignacio Romero, Mariana Inés Holubiec, Tamara Logica Tornatore, Stéphanie Rivière, Eva-Maria Hanschmann, Rodolfo Alberto Kölliker-Frers, Julia Tau, Eduardo Blanco, Pablo Galeano, Fernando Rodríguez de Fonseca, Christopher Horst Lillig, Francisco Capani
The general disruption of redox signaling following an ischemia-reperfusion episode has been proposed as a crucial component in neuronal death and consequently brain damage. Thioredoxin (Trx) family proteins control redox reactions and ensure protein regulation via specific, oxidative posttranslational modifications as part of cellular signaling processes. Trx proteins function in the manifestation, progression, and recovery following hypoxic/ischemic damage. Here, we analyzed the neuroprotective effects of postinjury, exogenous administration of Grx2 and Trx1 in a neonatal hypoxia/ischemia model...
2017: Oxidative Medicine and Cellular Longevity
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