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blood brain barrier damage ischemic

Michael J Poellmann, Jiyoon Bu, Seungpyo Hong
Ischemic stroke is a leading cause of death and disability worldwide and is in urgent need of new treatment options. The only approved treatment for stroke restores blood flow to the brain, but much of the tissue damage occurs during the subsequent reperfusion. Antioxidant therapies that directly address ischemia-reperfusion injury have shown promise in preclinical results. In this review, we discuss that reformulating antioxidant therapies as nanomedicine can potentially overcome the barriers that have kept these therapies from succeeding in the clinic...
October 4, 2018: Nanomedicine
Lu-Yao Ao, Yun-Yi Yan, Lin Zhou, Cheng-Yuan Li, Wan-Ting Li, Wei-Rong Fang, Yun-Man Li
Ischemic stroke is one of the leading health issues and the major cause of permanent disability in adults worldwide. Energy depletion and hypoxia occurring after ischemic stroke result in cell death, which activates resident glia cells and promotes the peripheral immune cells breaching into brain performing various functions even contradictory effects. The infiltration of immune cells may mediate neuron apoptosis and escalate ischemic damage, while it enhances neuron repair, differentiation, and neuroregeneration...
October 1, 2018: Journal of Molecular Neuroscience: MN
Olivera Rajkovic, Geoffrey Potjewyd, Emmanuel Pinteaux
Inflammation is a major pathological event following ischemic stroke that contributes to secondary brain tissue damage leading to poor functional recovery. Following the initial ischemic insult, post-stroke inflammatory damage is driven by initiation of a central and peripheral innate immune response and disruption of the blood-brain barrier (BBB), both of which are triggered by the release of pro-inflammatory cytokines and infiltration of circulating immune cells. Stroke therapies are limited to early cerebral blood flow reperfusion, and whilst current strategies aim at targeting neurodegeneration and/or neuroinflammation, innovative research in the field of regenerative medicine aims at developing effective treatments that target both the acute and chronic phase of inflammation...
2018: Frontiers in Neurology
Fangbin Chen, Zhiyang Liu, Wei Peng, Zhiqin Gao, Hui Ouyang, Tongjun Yan, Songbai Ding, Zhankui Cai, Bin Zhao, Longjin Mao, Zhiyong Cao
Vascular dementia (VD) is a syndrome characterized by progressive cognitive decline. According to previous studies, stroke is considered to be a risk factor for VD. The disruption of the blood-brain barrier (BBB) is pivotal to the pathology of stroke, as it contributes to post-stroke inflammation and edema. It has been reported that the Eph/Ephrin signaling pathway serves an important role in central nervous system injury. However, the role of EphrinA1/EphA4 signaling in BBB damage following ischemic stroke has not yet been reported...
September 2018: Experimental and Therapeutic Medicine
Dan Lu, Hong-Cheng Mai, Yu-Bin Liang, Bing-Dong Xu, An-Ding Xu, Yu-Sheng Zhang
Hemorrhage transformation is the most challenging preventable complication in thrombolytic therapy and is related to recombinant tissue plasminogen activator (rt-PA)-induced blood-brain barrier (BBB) damage. Intraperitoneal injections of normal or high doses of rosuvastatin were administered to Balb/c mice 20 min prior to middle cerebral artery occlusion (MCAO) surgery for 3 h followed by reperfusion with rt-PA thrombolytic therapy and cerebral blood flow monitoring to investigate whether a high or normal dose of rosuvastatin reduces BBB damage after brain ischemia and rt-PA reperfusion...
2018: Frontiers in Pharmacology
Yongtao Gao, Xiaobing Chen, Honglin Liu
A prospective resource of pharmacological treatment of ischemic brains stroke is rapid interference using potential neuroprotective materials. Cerium oxide nanoparticles have been shown to defend against blood brain barrier damage in cerebral ischemic brain stroke. While cerium oxide nanoparticles is highly permeable across the blood-brain barrier and also these nanoparticles are effective antioxidants, due to its ability to either donate or obtain electrons with alternative +3 and +4 valence states. This oxidation state of cerium oxide has shown efficiency in neutralizing generated free radicals in biological systems has been explored action for cerebral ischemic brain stroke...
October 2018: Journal of Photochemistry and Photobiology. B, Biology
Michelle A Erickson, Joseph A Nicolazzo, William A Banks
This year's 2018 Named Series on blood-brain interfaces highlights the importance of brain barriers as mediators of neuroimmune communication and regulators of neurological function. The term "brain interfaces" reflects our growing understanding that brain barriers such as the blood-brain barrier (BBB) and blood-CSF barrier (BCSFB) are not only gatekeepers, but facilitators of bidirectional communication between the brain and periphery. There is also an emerging appreciation that CNS sites that are exposed to blood-borne immune molecules and cells, such as the leptomeninges and circumventricular organs, may also be considered brain interfaces with important homeostatic and pathological functions...
August 30, 2018: Brain, Behavior, and Immunity
Miaodan Li, Shumin Chen, Xue Shi, Chenfei Lyu, Yongfang Zhang, Miaoqin Tan, Chen Wang, Nailiang Zang, Xiaoxi Liu, Yafang Hu, Jiangang Shen, Liang Zhou, Yong Gu
BACKGROUND: Blood-brain barrier (BBB) breakdown and inflammatory responses are the major causes of tissue-type plasminogen activator (tPA)-induced hemorrhagic transformation (HT), while high-mobility group box 1 (HMGB1) exacerbates inflammatory damage to BBB during the process of brain ischemia/reperfusion. This study aimed to investigate the change of HMGB1 after thrombolytic therapy and whether blocking HMGB1 could ameliorate the neurovasculature complications secondary to tPA treatment in stroke rats...
August 23, 2018: Journal of Neuroinflammation
Furong Ju, Yanli Ran, Lirui Zhu, Xiaofeng Cheng, Hao Gao, Xiaoxia Xi, Zhanli Yang, Shengxiang Zhang
Ischemic stroke can induce rapid disruption of blood-brain barrier (BBB). It has been suggested that increased BBB permeability can affect the pathological progression of ischemic tissue. However, the impact of increased BBB permeability on microglial activation and synaptic structures following reperfusion after ischemia remains unclear. In this study, we investigated microglial activation, dendritic damage and plasticity of dendritic spines after increasing BBB permeability following transient global cerebral ischemia in the somatosensory cortices in mice...
2018: Frontiers in Cellular Neuroscience
Dan Lu, Yanfang Liu, Hongcheng Mai, Jiankun Zang, Lingling Shen, Yusheng Zhang, Anding Xu
Hemorrhagic transformation (HT) is a serious complication that stimulates inflammation during reperfusion therapy after acute ischemic stroke. Rosuvastatin, a 3-hydroxymethyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, might improve the outcome of HT by inhibiting neuroinflammation. This study aimed to explore the protective effects of rosuvastatin against HT after recombinant tissue plasminogen activator (rt-PA) treatment in mice with experimental stroke via the attenuation of inflammation. A total of one hundred sixty-nine male BALB/c mice were used in the experiment...
2018: Frontiers in Cellular Neuroscience
Yongyan Yang, Beibei Dong, Jun Lu, Guolin Wang, Yonghao Yu
Ischemic stroke causes endothelial dysfunction and blood-brain barrier dysfunction, thus damages synaptic plasticity such as learning and memory. In this study we aim to investigate the effect of hemopexin (HPX) in protecting synaptic plasticity and blood brain barrier integrity from toxic heme, and determine whether this effect is via the activation of endothelial progenitor cells (EPCs) through the heme oxygenase-1(HO-1) pathway. Our data indicates HPX showed a significant effect in inducing the expression of HO-1, promoting the migration and differentiation of EPCs, facilitating new blood vessel formation thus protecting blood-brain barrier integrity...
August 6, 2018: Brain Research
Bao-Shuai Shan, Masaki Mogi, Jun Iwanami, Hui-Yu Bai, Harumi Kan-No, Akinori Higaki, Li-Juan Min, Masatsugu Horiuchi
The brain renin-angiotensin system plays a crucial role in ischemic stroke. It is known that stimulation of the angiotensin II type 2 (AT2 ) receptor protects against ischemic brain injury. We recently demonstrated that AT2 receptor stimulation by compound 21 (C21), a direct AT2 receptor agonist, inhibited vascular intimal proliferation with activation of peroxisome proliferator-activated receptor-gamma (PPAR-γ). However, whether direct AT2 receptor stimulation protects against ischemic brain injury via PPAR-γ activation is still unknown...
October 2018: Hypertension Research: Official Journal of the Japanese Society of Hypertension
Ting Zhang, Chang-Yan Li, Jing-Jing Jia, Jie-Shan Chi, Da Zhou, Jian-Zhou Li, Xiao-Ma Liu, Jun Zhang, Li Yi
Ischemia/reperfusion is known to greatly increase oxidative stress in the penumbra, which results in brain damage. Integrin αvβ3 is selectively up-regulated with ischemic injury to the brain and remains elevated throughout reperfusion. We determined whether or not a new compound biotinylated-LXW7-ceria nanoparticle (CeNP) (bLXW7-CeNP) plays a role in brain protection in the rat model of middle cerebral artery occlusion/reperfusion and shows better effects than CeNPs alone in improving the outcomes of focal oxidative stress and apoptosis more effectively...
February 2018: Current medical science
Zhiying Chen, Yuanyuan Xiang, Bing Bao, Xiangbin Wu, Zhongbin Xia, Jianyou You, Hongbing Nie
Cerebrovascular injury is the most prevalent human cerebrovascular disease and frequently results in ischemic stroke. Simvastatin may be a potential therapeutic agent for the treatment of patients with cerebrovascular injury. The present study aimed to investigate the efficacy of and the potential mechanisms regulated by simvastatin in a rat model of ischemia‑reperfusion (I/R)‑induced cerebrovascular injury. Cerebrovascular injury model rats were established and were subsequently treated with simvastatin or a vehicle control following I/R injury...
September 2018: Molecular Medicine Reports
Zareen Amtul, Carmen Frías, Jasmine Randhawa, David J Hill, Edith J Arany
The hippocampus, a brain region vital for memory and learning, is sensitive to the damage caused by ischemic/hypoxic stroke and is one of the main regions affected by Alzheimer's disease. The pathological changes that might occur in the hippocampus and its connections, because of cerebral injury in a distant brain region, such as the striatum, have not been examined. Therefore, in the present study, we evaluated the combined effects of endothelin-1-induced ischemia (ET1) in the striatum and β-amyloid (Aβ) toxicity on hippocampal pathogenesis, dictated by the anatomical and functional intra- and inter-regional hippocampal connections to the striatum...
July 28, 2018: Molecular Neurobiology
Manuel Navarro-Oviedo, Carmen Roncal, Agustina Salicio, Miriam Belzunce, Obdulia Rabal, Estefanía Toledo, Beatriz Zandio, Jose A Rodríguez, Jose A Páramo, Roberto Muñoz, Josune Orbe
Diabetes is an important risk factor for ischemic stroke (IS). Tissue-type plasminogen activator (tPA) has been associated with less successful revascularization and poor functional outcome in diabetes. We assessed whether a new thrombolytic strategy based on MMP10 was more effective than tPA in a murine IS model of streptozotocin (STZ)-induced diabetes. Wild-type mice were administered a single dose of streptozotocin (STZ) (180 mg/kg) to develop STZ-induced diabetes mellitus. Two weeks later, IS was induced by thrombin injection into the middle cerebral artery and the effect of recombinant MMP10 (6...
July 27, 2018: Translational Stroke Research
Hsiu-Mei Huang, Chao-Ching Huang, Meng-Han Tsai, Yi-Chieh Poon, Ying-Chao Chang
Purpose: Perinatal hypoxic-ischemic (HI) injury causes significant damages in the immature retina. The brain-derived neurotrophic factor is well known for its neuroprotective role but has limited clinical applications. A selective agonist of tyrosine kinase receptor B, 7,8-dihydroxyflavone (DHF), is a powerful therapeutic tool, when administered systemically. However, it remains unclear whether DHF treatment can protect the immature retinas against HI injury. Methods: Postnatal (P) day 7 rat pups were intraperitoneally injected with DHF or vehicle 2 hours before and 18 hours after being subjected to HI injury...
June 1, 2018: Investigative Ophthalmology & Visual Science
Jie Qu, Hengli Zhao, Qiang Li, Pengyu Pan, Kang Ma, Xin Liu, Hua Feng, Yujie Chen
Background: Mammalian sterile 20-like kinase 1 (MST1), the key component of the Hippo-YAP pathway, exhibits an important role in the pathophysiological process of various neurological disorders, including ischemic stroke and spinal cord injury. However, during subarachnoid hemorrhage, the involvement of MST1 in the pathophysiology of early brain injury remains unknown. Methods: We employed intravascular filament perforation to establish the subarachnoid hemorrhage (SAH) mouse model...
2018: Behavioural Neurology
Yijun Cheng, Jieyu Zan, Yaying Song, Guoyuan Yang, Hanbing Shang, Weiguo Zhao
Intestinal injury is a common complication following intracerebral hemorrhage (ICH), which leads to malnutrition, impaired immunity and unsatisfactory prognosis. Previous studies have revealed the pathogenesis of intestinal injury following traumatic brain injury using ischemic stroke models. However, the effects of ICH on intestinal injury remain unknown. The present study aimed to investigate the pathological alterations and molecular mechanism, as well as the time course of intestinal injury following ICH in mice...
October 2018: International Journal of Molecular Medicine
Yi-Fan Zhou, Peng-Cheng Li, Jie-Hong Wu, James Andrew Haslam, Ling Mao, Yuan-Peng Xia, Quan-Wei He, Xu-Xia Wang, Hao Lei, Xiao-Li Lan, Qing Robert Miao, Zhen-Yu Yue, Ya-Nan Li, Bo Hu
Brain tissue survival and functional recovery after ischemic stroke greatly depend on cerebral vessel perfusion and functional collateral circulation in the ischemic area. Semaphorin 3E (Sema3E), one of the class 3 secreted semaphorins, has been demonstrated to be a critical regulator in embryonic and postnatal vascular formation via binding to its receptor PlexinD1. However, whether Sema3E/PlexinD1 signaling is involved in poststroke neovascularization remains unknown. To determine the contribution of Sema3E/PlexinD1 signaling to poststroke recovery, aged rats (18 months) were subjected to a transient middle cerebral artery occlusion...
October 2018: Neurobiology of Aging
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