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cerebral ischemia mechanism

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https://www.readbyqxmd.com/read/28453486/cognitive-deficits-after-cerebral-ischemia-and-underlying-dysfunctional-plasticity-potential-targets-for-recovery-of-cognition
#1
Holly M Stradecki-Cohan, Charles H Cohan, Ami P Raval, Kunjan R Dave, Diego Reginensi, Rolando A Gittens, Mehdi Youbi, Miguel A Perez-Pinzon
Cerebral ischemia affects millions of people worldwide and survivors suffer from long-term functional and cognitive deficits. While stroke and cardiac arrest are typically considered when discussing ischemic brain injuries, there is much evidence that smaller ischemic insults underlie neurodegenerative diseases, including Alzheimer's disease. The "regenerative" capacity of the brain relies on several aspects of plasticity that are crucial for normal functioning; less affected brain areas may take over function previously performed by irreversibly damaged tissue...
April 25, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28442781/spreading-depolarization-remarkably-exacerbates-ischemia-induced-tissue-acidosis-in-the-young-and-aged-rat-brain
#2
Ákos Menyhárt, Dániel Zölei-Szénási, Tamás Puskás, Péter Makra, M Tóth Orsolya, Borbála É Szepes, Réka Tóth, Orsolya Ivánkovits-Kiss, Tihomir P Obrenovitch, Ferenc Bari, Eszter Farkas
Spreading depolarizations (SDs) occur spontaneously in the cerebral cortex of subarachnoid hemorrhage, stroke or traumatic brain injury patients. Accumulating evidence prove that SDs exacerbate focal ischemic injury by converting zones of the viable but non-functional ischemic penumbra to the core region beyond rescue. Yet the SD-related mechanisms to mediate neurodegeneration remain poorly understood. Here we show in the cerebral cortex of isoflurane-anesthetized, young and old laboratory rats, that SDs propagating under ischemic penumbra-like conditions decrease intra and- extracellular tissue pH transiently to levels, which have been recognized to cause tissue damage...
April 25, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28440874/role-of-glycogen-synthase-kinase-3-in-ischemia-induced-blood-brain-barrier-disruption-in-aged-female-rats
#3
Han Xiao, Mingyang Deng, Binbin Yang, Jianguang Tang, Zhiping Hu
Estrogen receptors have protective effects against ischemic brain injury. However, the molecular mechanisms underlying this phenomenon have yet to be well studied. Given that inhibition of glycogen synthase kinase (GSK3) can reduce cerebral ischemia/reperfusion injury, we hypothesized that estrogen receptors-mediated protective effects against ischemia-induced blood brain barrier (BBB) disruption involve inhibition of GSK3. Thus, we evaluated GSK3 expression in the brain of ovariectomized female rats, and examined the effects of intracerebroventricular pre-treatments of SB216763, GSK3 inhibitor, on BBB permeability following middle cerebral artery occlusion (MCAO)...
April 25, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28439774/albumin-induced-neuroprotection-in-focal-cerebral-ischemia-in-the-alias-trial-does-severity-mechanism-and-time-of-infusion-matter
#4
Rakesh Khatri, Mohammad Rauf Afzal, Gustavo J Rodriguez, Alberto Maud, Muhammad Shah Miran, Mohtashim Arbaab Qureshi, Salvador Cruz-Flores, Adnan I Qureshi
OBJECTIVE: To determine whether there is any differential benefit of albumin administration within 2 h of onset of ischemia and in settings (severe ischemia with reperfusion in cardioembolic strokes with National Institutes of Health Stroke Scale [NIHSS] ≥15), most representative of experimental models of cerebral ischemia in which albumin was effective in reducing neurological injury. BACKGROUND: High-dose intravenous (IV) albumin treatment for acute ischemic stroke (ALIAS) trial did not show overall clinical benefit in ischemic stroke patients in contrast to preclinical studies; however, models of preclinical studies were not completely followed...
April 24, 2017: Neurocritical Care
https://www.readbyqxmd.com/read/28438516/global-transcriptomic-profiling-of-cortex-and-striatum-cerebral-injury-after-ischemia-reperfusion-in-a-mouse-model
#5
Zhenying Zhao, Zhiqiang Lu, Xiuying Sun, Tianhong Zhao, Jihong Zhang, Cunxia Zhou, Xiaohui Zheng, Huijuan Zhang, Guiling Shi
OBJECTIVE: This study aims to investigate the molecular mechanism of injury development in the cortex and the striatum after cerebral ischemia/reperfusion (I/R). METHODS: Gene expression data (GSE23160) in the cortex and the striatum of an intraluminal middle cerebral artery occlusion-I/R mouse model (N = 12) and sham controls (N = 4) were downloaded from the Gene Expression Omnibus. Limma package was used to identify the differentially expressed genes (DEGs) between the I/R (2, 8, and 24 hours) and control groups...
April 21, 2017: Journal of Stroke and Cerebrovascular Diseases: the Official Journal of National Stroke Association
https://www.readbyqxmd.com/read/28433650/long-noncoding-rna-malat1-is-a-potent-autophagy-inducer-protecting-brain-microvascular-endothelial-cells-against-oxygen-glucose-deprivation-reoxygenation-induced-injury-by-sponging-mir-26b-and-upregulating-ulk2-expression
#6
Zhijun Li, Jing Li, Na Tang
Brain microvascular endothelial cell (BMEC) injury induced by ischemia-reperfusion (I/R) is the initial stage of blood-brain barrier (BBB) disruption, which results in a poor prognosis in ischemic stroke patients. Autophagy has been shown to have protective effects on BMECs against cerebral ischemic insults. However, molecular mechanism of BMEC autophagy during I/R is unclear. Long noncoding RNAs (lncRNAs) are emerging as new factors involved in cell autophagy. LncRNA Malat1 is one of the most highly upregulated I/R or OGD/R-responsive endothelial lncRNA and plays a protective role in BMECs against cerebral ischemic insults...
April 20, 2017: Neuroscience
https://www.readbyqxmd.com/read/28428752/desensitizing-mitochondrial-permeability-transition-by-erk-cyclophilin-d-axis-contributes-to-the-neuroprotective-effect-of-gallic-acid-against-cerebral-ischemia-reperfusion-injury
#7
Jing Sun, Da-Dui Ren, Jin-Yi Wan, Chen Chen, Dong Chen, Huan Yang, Chun-Lai Feng, Jing Gao
Ischemic stroke is a devastating disease with complex pathophysiology. Much evidence confirms that opening of the mitochondrial permeability transition pore (MPTP) is related with mitochondrial dysfunction to apoptosis in ischemic stroke, thus elucidating its signaling mechanism and screening novel MPTP inhibitor is therefore of paramount importance. Our earlier studies identified that gallic acid (GA), a naturally occurring plant phenol, endows with effect on inhibition of mitochondrial dysfunction, which has significant neuroprotective effect in cerebral ischemia/reperfusion injury...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28427869/ischemic-preconditioning-with-ketogenic-diet-improves-brain-ischemic-tolerance-through-increased-extracellular-adenosine-levels-and-hypoxia-inducible-factors
#8
Qi Yang, Min Guo, Xun Wang, Yanxin Zhao, Hongyan Ding, Mei Cui, Qiang Dong
Achieving a prolonged neuroprotective state reduces brain damage and neurological dysfunction characteristic of brain ischemia. The ketogenic diet (KD) has disease-modifying effects in several neurodegenerative disorders. In this study, we fed mice with KD for three weeks and performed reversible middle cerebral artery occlusion (MCAO) in the animals. KD-fed mice had significantly reduced infarct volume, increased regional cerebral blood flow (rCBF) and extracellular adenosine levels in both ischemic and reperfusion stages...
April 18, 2017: Brain Research
https://www.readbyqxmd.com/read/28421304/increased-autophagic-degradation-contributes-to-the-neuroprotection-of-hydrogen-sulfide-against-cerebral-ischemia-reperfusion-injury
#9
Yuanjun Zhu, Mengyang Shui, Xiaoyan Liu, Wenhui Hu, Yinye Wang
Hydrogen sulfide (H2S), an endogenous gaseous signal molecule, exhibits protective effect against ischemic injury. However, its underlying mechanism is not fully understood. We have recently reported that exogenous H2S decreases the accumulation of autophagic vacuoles in mouse brain with ischemia/reperfusion (I/R) injury. To further investigate whether this H2S-induced reduction of autophagic vacuoles is caused by the decreased autophagosome synthesis and/or the increased autophagic degradation inautophagic flux, we performed in vitro and in vivo studies using SH-SY5Y cells for the oxygen and glucose deprivation/reoxygenation (OGD/R) and mice for the cerebral I/R, respectively...
April 18, 2017: Metabolic Brain Disease
https://www.readbyqxmd.com/read/28421173/cerebral-autoregulation-brain-injury-and-the-transitioning-premature-infant
#10
REVIEW
Zachary A Vesoulis, Amit M Mathur
Improvements in clinical management of the preterm infant have reduced the rates of the two most common forms of brain injury, such as severe intraventricular hemorrhage and white matter injury, both of which are contributory factors in the development of cerebral palsy. Nonetheless, they remain a persistent challenge and are associated with a significant increase in the risk of adverse neurodevelopment outcomes. Repeated episodes of ischemia-reperfusion represent a common pathway for both forms of injury, arising from discordance between systemic blood flow and the innate regulation of cerebral blood flow in the germinal matrix and periventricular white matter...
2017: Frontiers in Pediatrics
https://www.readbyqxmd.com/read/28419850/overpressure-blast-injury-induced-oxidative-stress-and-neuroinflammation-response-in-rat-frontal-cortex-and-cerebellum
#11
Hale Z Toklu, Zhihui Yang, Sehkar Oktay, Yasemin Sakarya, Nataliya Kirichenko, Michael K Matheny, Judy Muller-Delp, Kevin Strang, Philip J Scarpace, Kevin K W Wang, Nihal Tümer
BACKGROUND & AIM: Overpressure blast-wave induced brain injury (OBI) and its long-term neurological outcome pose significant concerns for military personnel. Our aim is to investigate the mechanism of injury due to OBI. METHODS: Rats were divided into 3 groups: 1) Control, 2) OBI (exposed 30psi peak pressure, 2-2.5ms), 3) Repeated OBI (r-OBI) (three exposures over one-week period). Lung and brain (cortex and cerebellum) tissues were collected at 24h post injury...
April 15, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28417216/pathogenic-mechanisms-following-ischemic-stroke
#12
REVIEW
Seyed Esmaeil Khoshnam, William Winlow, Maryam Farzaneh, Yaghoob Farbood, Hadi Fathi Moghaddam
Stroke is the second most common cause of death and the leading cause of disability worldwide. Brain injury following stroke results from a complex series of pathophysiological events including excitotoxicity, oxidative and nitrative stress, inflammation, and apoptosis. Moreover, there is a mechanistic link between brain ischemia, innate and adaptive immune cells, intracranial atherosclerosis, and also the gut microbiota in modifying the cerebral responses to ischemic insult. There are very few treatments for stroke injuries, partly owing to an incomplete understanding of the diverse cellular and molecular changes that occur following ischemic stroke and that are responsible for neuronal death...
April 17, 2017: Neurological Sciences
https://www.readbyqxmd.com/read/28414101/autophagy-in-hemorrhagic-stroke-mechanisms-and-clinical-implications
#13
REVIEW
Haiying Li, Jiang Wu, Haitao Shen, Xiyang Yao, Chenglin Liu, S Pianta, J Han, C V Borlongan, Gang Chen
Accumulating evidence advances the critical role of autophagy in brain pathology after stroke. Investigations employing autophagy induction or inhibition using pharmacological tools or autophagy-related gene knockout mice have recently revealed the biological significance of intact and functional autophagy in stroke. Most of the reported cases attest to a pro-survival role for autophagy in stroke, by facilitating removal of damaged proteins and organelles, which can be recycled for energy generation and cellular defenses...
April 13, 2017: Progress in Neurobiology
https://www.readbyqxmd.com/read/28413924/erythropoietin-attenuates-axonal-injury-after-middle-cerebral-artery-occlusion-in-mice
#14
Rongliang Wang, Haiping Zhao, Jincheng Li, Yunxia Duan, Zhibin Fan, Zhen Tao, Fei Ju, Feng Yan, Yumin Luo
OBJECTIVE: Erythropoietin (EPO) confers potent neuroprotection against ischemic injury through a variety of mechanisms. However, the protective effect of EPO on axons after cerebral ischemia in adult mice is rarely covered. The purpose of this study was to investigate the potential neuroprotective effects of EPO on axons in mice after cerebral ischemia. METHODS: A total of 30 adult male C57 BL/6 mice were treated with EPO (5000 IU/kg) or vehicle after transient middle cerebral artery occlusion (MCAO)...
April 16, 2017: Neurological Research
https://www.readbyqxmd.com/read/28413461/long-noncoding-rna-malat1-inhibits-apoptosis-induced-by-oxygen-glucose-deprivation-and-reoxygenation-in-human-brain-microvascular-endothelial-cells
#15
Jia-Wei Xin, Yu-Gang Jiang
Cerebral ischemia/reperfusion (I/R) injury leads to brain vascular dysfunction, which is characterized by endothelial cell injury or death. Long noncoding (lnc) RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is reportedly associated with endothelial cell functions and dysfunctions. In the present study, the role of MALAT1 in I/R-induced cerebral vascular endothelial cell apoptosis was explored using oxygen-glucose deprivation and reoxygenation (OGD-R) as an in vitro I/R injury model. Primary human brain microvascular endothelial cells were cultured under OGD-R, and the expression levels of MALAT1 and cell apoptosis were measured at 6, 9, 12, 24 and 36 h post-reoxygenation...
April 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28408940/laser-acupuncture-exerts-neuroprotective-effects-via-regulation-of-creb-bdnf-bcl-2-and-bax-gene-expressions-in-the-hippocampus
#16
Yeong-Chan Yun, Dongyeop Jang, Sun-Bee Yoon, Dohyeong Kim, Dong-Hee Choi, O-Sang Kwon, Yu-Mi Lee, Daehwan Youn
Acupuncture has a positive effect on cognitive deficits. However, the effects of laser acupuncture (LA) on cognitive function and its mechanisms of action are unclear. The present study aimed to evaluate the effects of LA on middle cerebral artery occlusion- (MCAO-) induced cognitive impairment and its mechanisms of action. Transient focal cerebral ischemia was modeled in adult Sprague-Dawley rats by MCAO. After LA or manual-acupuncture (MA) treatment at the GV20 and HT7 for 2 weeks, hippocampal-dependent memory was evaluated using the Morris water maze (MWM) test...
2017: Evidence-based Complementary and Alternative Medicine: ECAM
https://www.readbyqxmd.com/read/28407836/-role-of-c-jun-n-terminal-kinase-mediated-foxo3a-nuclear-translocation-in-neuronal-apoptosis-in-neonatal-rats-with-hypoxic-ischemic-brain-damage
#17
De-Yuan Li, Jin-Lin Wu, Li-Li Luo, Li-Na Qiao, Zhong-Qiang Liu, Guo-Yan Lu, Yang Wang
OBJECTIVE: To explore the mechanisms of neuroprotective effects of c-Jun N-terminal kinase (JNK)/FOXO3a transcription factor signaling pathway inhibition on hypoxic-ischemic neuronal apoptosis in neonatal rats with hypoxic-ischemic brain damage (HIBD). METHODS: Sixty-four 7-day-old Sprague-Dawley rats were divided into four groups: hypoxia-ischemia (HI), sham-operated, JNK specific inhibitor AS601245-treated, and DMSO vehicle. Rats' cerebral cortexes were collected at 24 hours after HI...
April 2017: Zhongguo Dang Dai Er Ke za Zhi, Chinese Journal of Contemporary Pediatrics
https://www.readbyqxmd.com/read/28401402/ischemia-reperfusion-induced-translocation-of-pkc%C3%AE-ii-to-mitochondria-as-an-important-mediator-of-a-protective-signaling-mechanism-in-an-ischemia-resistant-region-of-the-hippocampus
#18
Olga Krupska, Anna Sarnowska, Bartlomiej Fedorczyk, Magdalena Gewartowska, Aleksandra Misicka, Barbara Zablocka, Malgorzata Beresewicz
Emerging reports indicate that activated PKC isoforms that translocate to the mitochondria are pro- or anti-apoptotic to mitochondrial function. Here, we concentrate on the role of PKCβ translocated to mitochondria in relation to the fate of neurons following cerebral ischemia. As we have demonstrated previously ischemia/reperfusion injury (I/R) results in translocation of PKCβ from cytoplasm to mitochondria, but only in ischemia-resistant regions of the hippocampus (CA2-4, DG), we hypothesize that this translocation may be a mediator of a protective signaling mechanism in this region...
April 12, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28400806/a-protease-activated-receptor-1-antagonist-protects-against-global-cerebral-ischemia-reperfusion-injury-after-asphyxial-cardiac-arrest-in-rabbits
#19
Jing-Ning Yang, Jun Chen, Min Xiao
Cerebral ischemia/reperfusion injury is partially mediated by thrombin, which causes brain damage through protease-activated receptor 1 (PAR1). However, the role and mechanisms underlying the effects of PAR1 activation require further elucidation. Therefore, the present study investigated the effects of the PAR1 antagonist SCH79797 in a rabbit model of global cerebral ischemia induced by cardiac arrest. SCH79797 was intravenously administered 10 minutes after the model was established. Forty-eight hours later, compared with those administered saline, rabbits receiving SCH79797 showed markedly decreased neuronal damage as assessed by serum neuron specific enolase levels and less neurological dysfunction as determined using cerebral performance category scores...
February 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/28400805/3-daidzein-sulfonate-sodium-improves-mitochondrial-functions-after-cerebral-ischemia-reperfusion-injury
#20
Wa Yuan, Qin Chen, Jing Zeng, Hai Xiao, Zhi-Hua Huang, Xiao Li, Qiong Lei
3'-Daidzein sulfonate sodium is a new synthetic water-soluble compound derived from daidzein (an active ingredient of the kudzu vine root). It has been shown to have a protective effect on cerebral ischemia/reperfusion injury in rats. We plan to study the mechanism of its protective effect. 3'-Daidzein sulfonate sodium was injected in rats after cerebral ischemia/reperfusion injury. Results showed that 3'-daidzein sulfonate sodium significantly reduced mitochondrial swelling, significantly elevated the mitochondrial membrane potential, increased mitochondrial superoxide dismutase and glutathione peroxidase activities, and decreased mitochondrial malondialdehyde levels...
February 2017: Neural Regeneration Research
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