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https://www.readbyqxmd.com/read/28810591/dual-character-of-flavonoids-in-attenuating-and-aggravating-ischemia-reperfusion-induced-myocardial-injury
#1
Wenqiang Li, Yun Li, Ruifang Sun, Sumei Zhou, Meifeng Li, Mingchen Feng, Yingguang Xie
The concept that flavonoids exert cardioprotection against myocardial ischemia-reperfusion (I/R) injury has been acknowledged by a large body of evidence. However, recent studies reported cardiotoxic effects of certain flavonoids, while the underlying mechanisms have remained largely elusive. Flavonoids have been demonstrated to activate aryl hydrocarbon receptor (Ahr), which is implicated in an array of cell signaling processes. The present study examined the cardioprotective roles of quercetin (Qu) and β-naphthoflavone (β-NF) against I/R injury and explored whether the underlying mechanism proceeds via molecular signaling downstream of Ahr...
August 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28807664/social-interaction-modulates-the-neuroinflammatory-response-to-global-cerebral-ischemia-in-male-mice
#2
Monica M Gaudier-Diaz, Ning Zhang, Adam H Haines, Surbhi, Min Zhou, A Courtney DeVries
Social isolation is a risk factor for cardiovascular and cerebrovascular diseases, although the underlying mechanisms remain underspecified. Considering the potential of microglia to become sensitized by stressors and their role in neuroinflammation, we hypothesized that social isolation primes microglia, resulting in an exaggerated neuroimmune response to experimental cerebral ischemia. First, major histocompatibility complex II (MHC II) gene expression, an indicator of microglial priming, was compared between mice that were socially isolated or pair-housed...
August 11, 2017: Brain Research
https://www.readbyqxmd.com/read/28804561/upregulation-of-mir-130b-protects-against-cerebral-ischemic-injury-by-targeting-water-channel-protein-aquaporin-4-aqp4
#3
Yueying Zheng, Liqing Wang, Manli Chen, Aijie Pei, Liwei Xie, Shengmei Zhu
Altered microRNA regulation has been implicated in the pathogenesis of various disorders, including cerebral ischemia/reperfusion injury (I/RI). However, the regulatory mechanism of miR-130b in cerebral ischemia injury has not been reported. In this study, we explored the role of miR-130b in cerebral ischemia injury and investigated its potential mechanism. Levels of miR-130b were quantified by real-time PCR, and the protein level of AQP4 was detected by Western blotting. Cell apoptosis was detected by flow cytometry...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28803066/a-novel-ripk1-inhibitor-that-prevents-retinal-degeneration-in-a-rat-glaucoma-model
#4
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/28795674/-effect-of-autophagy-regulator-on-the-injury-of-rat-hippocampal-neurons-induced-by-oxygen-glucose-deprivation
#5
Tianen Zhou, Chaotao Zeng, Jiajun Fang, Longyuan Jiang, Tao Yu
OBJECTIVE: To explore the effect of autophagy regulator on the injury of rat hippocampal neurons induced by oxygen-glucose deprivation (OGD). METHODS: Rat hippocampal neurons were cultivated in primary and subjected to OGD to simulate neuronal hypoxic ischemia injury for 2 hours or 6 hours followed by reperfusion for 12 hours with or without 3-methyladenine (3-MA, 20 μmol/L) or rapamycin (0.2 μmol/L). The morphology of neurons was observed with optical microscope...
August 2017: Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
https://www.readbyqxmd.com/read/28790819/kalopanacis-cortex-extract-capped-gold-nanoparticles-activate-nrf2-signaling-and-ameliorate-damage-in-human-neuronal-sh-sy5y-cells-exposed-to-oxygen-glucose-deprivation-and-reoxygenation
#6
Sun Young Park, Seon Yeong Chae, Jin Oh Park, Kyu Jin Lee, Geuntae Park
Recently, environment-friendly synthesis of gold nanoparticles (GNPs) has been extensively explored by biologists and chemists. However, significant research is still required to determine whether "eco-friendly" GNPs are beneficial to human health and to elucidate the molecular mechanisms of their effects on human cells. We used human neuronal SH-SY5Y cells to show that treatment with Kalopanacis Cortex extract-capped GNPs (KC-GNs), prepared via an eco-friendly, fast, one-pot synthetic route, protected neuronal cells against oxygen-glucose deprivation/reoxygenation (OGD/R)-induced damage...
2017: International Journal of Nanomedicine
https://www.readbyqxmd.com/read/28780351/down-regulation-of-lncrna-kcnq1ot1-protects-against-myocardial-ischemia-reperfusion-injury-following-acute-myocardial-infarction
#7
Xin Li, Yingnan Dai, Shujun Yan, Yanli Shi, Baihe Han, Jingxiu Li, Li Cha, Jianjun Mu
This study aimed to investigate the protective effects of long non-coding RNA KCNQ1OT1 against myocardial ischemia/reperfusion (I/R) injury following acute myocardial infarction, as well as its regulatory mechanism. We used the cardiac muscle H9c2 cells under condition of oxygen glucose deprivation followed by reperfusion (OGD/R) to induce myocardial I/R injury. Then H9C2 cells were transfected with si-NC, si-KCNQ1OT1, pc-NC, pc-KCNQ1OT1, si-AdipoR1 and si-AdipoR2, respectively. The myocardial cell viability and apoptosis were respectively detected...
August 2, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28774372/-expression-rhythm-of-autophagic-gene-in-neurons-of-neonatal-rats-with-hypoxia-ischemia-and-its-regulatory-mechanism
#8
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/28765953/atorvastatin-protects-cardiomyocytes-against-ogd-r%C3%A2-induced-apoptosis-by-inhibiting-mir%C3%A2-199a%C3%A2-5p
#9
Yong Li, Ting Jiang, Xingli Fu, Hao Xu, Jianguo Ji
The present study aimed to evaluate the protective effects of atorvastatin against myocardial ischemia/reperfusion (I/R) injury in cardiomyocytes and its underlying mechanisms. The direct cytotoxic effects of oxygen‑glucose deprivation/reperfusion (OGD/R) on cardiomyocytes with and without atorvastatin pretreatment were evaluated. The effects of atorvastatin on the expression of glycogen synthase kinase‑3β (GSK‑3β) and microRNA (miR)‑199a‑5p were determined using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analyses...
July 25, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28751019/the-cystathionine-%C3%AE-synthase-hydrogen-sulfide-pathway-contributes-to-microglia-mediated-neuroinflammation-following-cerebral-ischemia
#10
Minjie Zhang, Xiaowei Wu, Yingxiu Xu, Meijun He, Jiaying Yang, Jie Li, Yuyao Li, Guizhen Ao, Jian Cheng, Jia Jia
The mechanisms underlying neuroinflammation following cerebral ischemia remain unclear. Hydrogen sulfide (H2S), a newly identified gasotransmitter, has been reported to regulate inflammation. In the current study, we investigated whether the endogenous H2S production pathway contributed to microglia-mediated neuroinflammation following stroke. We used a mouse middle cerebral artery occlusion (MCAO) model and an in vitro cellular model to mimic ischemia-induced microglial neuroinflammation. Expression of the H2S synthase cystathionine β-synthase (CBS) and H2S synthetic activity were rapidly decreased in the ischemic brain tissue following MCAO...
July 24, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28747335/crosstalk-between-intracellular-zinc-rises-and-reactive-oxygen-species-accumulation-in-chemical-ischemia
#11
Kira G Slepchenko, Qiping Lu, Yang V Li
Both zinc (Zn(2+)) and reactive oxygen species (ROS) have been shown to accumulate during hypoxic-ischemic stress and play important roles in pathological processes. Here we studied Zn(2+) and ROS accumulations by employing fluorescent probes in HeLa cells to further the understanding of cause and effect relationship of these two important cellular signaling during chemical-ischemia, stimulated by oxygen and glucose deprivation (OGD). We observed two Zn(2+) rises that were divided into four phases in the course of 30 minutes OGD...
July 26, 2017: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/28743390/baicalin-attenuates-in-vivo-and-in-vitro-hyperglycemia-exacerbated-ischemia-reperfusion-injury-by-regulating-mitochondrial-function-in-a-manner-dependent-on-ampk
#12
Shanshan Li, Xiaoxu Sun, Lixing Xu, Ruoxi Sun, Zhanqiang Ma, Xueyang Deng, Baolin Liu, Qiang Fu, Rong Qu, Shiping Ma
Cerebral ischemia/reperfusion (I/R) is a lethal and disabling disease. Studies have suggested that hyperglycemia is a risk factor for cerebral I/R. Baicalin is a natural bioactive flavonoid extracted from Scutellaria baicalensis Georgi with neuroprotective activity. In the present study, we investigated the effects of baicalin on hyperglycemia-exacerbated cerebral I/R injury. Streptozotocin (STZ) injection aggravated the brain damage induced by middle cerebral artery occlusion (MCAO) surgery, while baicalin administration reduced blood glucose, relieved neurological deficit and decreased infarct volume...
July 22, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28732772/a-brain-specific-isoform-of-apoptosis-inducing-factor-2-attenuates-ischemia-induced-oxidative-stress-in-ht22-cells
#13
Yuanyang Xie, Siyi Wanggou, Qing Liu, Xuejun Li, Jingping Liu, Ming Wu
Apoptosis-inducing factor (AIF) is a family of conserved mitochondrial flavoproteins that have both vital and lethal functions in cells. The function and regulation of AIF-1, the original described and most abundant isoform, has been extensively studied, whereas three other AIF isoforms have not been further characterized. Here, we investigated the role of AIF-2, a brain-specific isoform of AIF, in an in vitro ischemia model in neuronal HT22 cells. We showed that AIF-2 was constitutively expressed in HT22 cells, and the oxygen and glucose deprivation (OGD) did not alter AIF-2 expression...
July 18, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28731692/quinolinyl-nitrone-rp19-induces-neuroprotection-after-transient-brain-ischemia
#14
Maria I Ayuso, Emma Martínez-Alonso, Mourad Chioua, Alejandro Escobar-Peso, Rafael Gonzalo-Gobernado, Joan Montaner, José Marco-Contelles, Alberto Alcázar
There is a need to develop additional effective therapies for ischemic stroke. Nitrones, which were first developed as reactive oxygen species (ROS)-trapping compounds, have been proposed as neuroprotective agents for ischemic stroke, a ROS-related disorder. The previous reported ROS-trapping compound, quinolyl nitrone RP19, is here being assayed to induce neuroprotection to ischemia-reperfusion injury in three experimental ischemia models: (i) oxygen-glucose deprivation (OGD) on primary neuronal cultures; (ii) transient global cerebral ischemia in four-vessel occlusion model; and (iii) transient focal cerebral ischemia in middle cerebral artery occlusion (tMCAO) model...
August 9, 2017: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/28729825/dexmedetomidine-protects-mouse-brain-from-ischemia-reperfusion-injury-via-inhibiting-neuronal-autophagy-through-up-regulating-hif-1%C3%AE
#15
Cong Luo, Ming-Wen Ouyang, Ying-Ying Fang, Shu-Ji Li, Quan Zhou, Jun Fan, Zai-Sheng Qin, Tao Tao
Stroke is the leading cause of death in China and produces a heavy socio-economic burden in the past decades. Previous studies have shown that dexmedetomidine (DEX) is neuroprotective after cerebral ischemia. However, the role of autophagy during DEX-mediated neuroprotection after cerebral ischemia is still unknown. In this study, we found that post-conditioning with DEX and DEX+3-methyladenine (3-MA) (autophagy inhibitor) reduced brain infarct size and improved neurological deficits compared with DEX+RAPA (autophagy inducer) 24 h after transient middle cerebral artery artery occlusion (tMCAO) model in mice...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28729821/optimized-model-of-cerebral-ischemia-in-situ-for-the-long-lasting-assessment-of-hippocampal-cell-death
#16
Oksana Rybachuk, Olga Kopach, Volodymyr Krotov, Nana Voitenko, Tatyana Pivneva
Among all the brain, the hippocampus is the most susceptible region to ischemic lesion, with the highest vulnerability of CA1 pyramidal neurons to ischemic damage. This damage may cause either prompt neuronal death (within hours) or with a delayed appearance (over days), providing a window for applying potential therapies to reduce or prevent ischemic impairments. However, the time course when ischemic damage turns to neuronal death strictly depends on experimental modeling of cerebral ischemia and, up to now, studies were predominantly focused on a short time-window-from hours to up to a few days post-lesion...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28726275/cpkc%C3%AE-mediated-down-regulation-of-uchl1-alleviates-ischaemic-neuronal-injuries-by-decreasing-autophagy-via-erk-mtor-pathway
#17
Dan Zhang, Song Han, Shizun Wang, Yanlin Luo, Li Zhao, Junfa Li
Stroke is one of the leading causes of death in the world, but its underlying mechanisms remain unclear. Both conventional protein kinase C (cPKC)γ and ubiquitin C-terminal hydrolase L1 (UCHL1) are neuron-specific proteins. In the models of 1-hr middle cerebral artery occlusion (MCAO)/24-hr reperfusion in mice and 1-hr oxygen-glucose deprivation (OGD)/24-hr reoxygenation in cortical neurons, we found that cPKCγ gene knockout remarkably aggravated ischaemic injuries and simultaneously increased the levels of cleaved (Cl)-caspase-3 and LC3-I proteolysis product LC3-II, and the ratio of TUNEL-positive cells to total neurons...
July 20, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28724924/neuron-autonomous-transcriptome-changes-upon-ischemia-reperfusion-injury
#18
Jinlong Shi, Xia Chen, Haiying Li, Youjia Wu, Shouyan Wang, Wei Shi, Jian Chen, Yaohui Ni
Ischemic stroke and the following reperfusion, an acute therapeutic intervention, can cause irreversible brain damages. However, the underlying pathological mechanisms are still under investigation. To obtain a comprehensive, real-time view of the cell-autonomous mechanisms involved in ischemic stroke and reperfusion, we applied the next-generation sequencing (NGS) technology to characterize the temporal changes in gene expression profiles using primarily cultured hippocampal neurons under an oxygen-glucose deprivation/reperfusion (OGD/R) condition...
July 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28724891/hypoxia-inducible-factor-1-alpha-is-involved-in-rip-induced-necroptosis-caused-by-in-vitro-and-in-vivo-ischemic-brain-injury
#19
Xiao-Sa Yang, Tai-Long Yi, Sai Zhang, Zhong-Wei Xu, Ze-Qi Yu, Hong-Tao Sun, Cheng Yang, Yue Tu, Shi-Xiang Cheng
Necroptosis, a novel type of programmed cell death, is involved in stroke-induced ischemic brain injury. Although studies have sought to explore the mechanisms of necroptosis, its signaling pathway has not yet to be completely elucidated. Thus, we used oxygen-glucose deprivation (OGD) and middle cerebral artery occlusion (MCAO) models mimicking ischemic stroke (IS) conditions to investigate mechanisms of necroptosis. We found that OGD and MCAO induced cell death, local brain ischemia and neurological deficit, while zVAD-fmk (zVAD, an apoptotic inhibitor), GSK'872 (a receptor interacting protein kinase-3 (RIP3) inhibitor), and combined treatment alleviated cell death and ischemic brain injury...
July 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28721600/resveratrol-ameliorates-hypoxia-ischemia-induced-brain-injury-in-the-neonatal-rat-via-the-mir-96-bax-axis
#20
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
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