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Cerebral ischemia protection

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https://www.readbyqxmd.com/read/28931617/normobaric-hyperoxia-reduces-blood-occludin-fragments-in-rats-and-patients-with-acute-ischemic-stroke
#1
Shuhai Shi, Zhifeng Qi, Qingfeng Ma, Rong Pan, Graham S Timmins, Yongmei Zhao, Wenjuan Shi, Yunzhou Zhang, Xunming Ji, Ke Jian Liu
BACKGROUND AND PURPOSE: Damage of the blood-brain barrier (BBB) increases the incidence of neurovascular complications, especially for cerebral hemorrhage after tPA (tissue-type plasminogen activator) therapy. Currently, there is no effective method to evaluate the extent of BBB damage to guide tPA use. Herein, we investigated whether blood levels of tight junction proteins could serve as biomarker of BBB damages in acute ischemic stroke (AIS) in both rats and patients. We examined whether this biomarker could reflect the extent of BBB permeability during cerebral ischemia/reperfusion and the effects of normobaric hyperoxia (NBO) on BBB damage...
September 20, 2017: Stroke; a Journal of Cerebral Circulation
https://www.readbyqxmd.com/read/28919157/ethyl-acetate-fraction-of-trichilia-catigua-restores-long-term-retrograde-memory-and-reduces-oxidative-stress-and-inflammation-after-global-cerebral-ischemia-in-rats
#2
Jacqueline Godinho, Rúbia Maria Weffort de Oliveira, Anacharis Babeto de Sa-Nakanishi, Cristiano Correia Bacarin, Claudia Hitomi Huzita, Renata Longhini, João Carlos P Mello, Celso Vataru Nakamura, Isolde Santos Previdelli, Matheus Henrique Dal Molin Ribeiro, Humberto Milani
We originally reported that an ethyl-acetate fraction (EAF) of Trichilia catigua prevented the impairment of water maze learning and hippocampal neurodegeneration after transient global cerebral (TGCI) in mice. We extended that previous study by evaluating whether T. catigua (i) prevents the loss of long-term retrograde memory assessed in the aversive radial maze (AvRM), (ii) confers hippocampal and cortical neuroprotection, and (iii) mitigates oxidative stress and neuroinflammation in rats that are subjected to the four vessel occlusion (4-VO) model of TGCI...
September 14, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28918255/microglia-mediated-baff-baffr-ligation-promotes-neuronal-survival-in-brain-ischemia-injury
#3
Kai Li, Wei Yu, Rangjuan Cao, Zhihua Zhu, Guoqing Zhao
The innate immune responses of brain to vascular occlusion are primarily orchestrated by activated microglia. However, the roles of microglia in inflammatory responses to brain ischemic injuries are controversial. Here, we report a new mechanism by which microglia confer protective effects on ischemic neuronal cells. We found that under ischemic condition, the B-cell activating factor (BAFF) was vastly upregulated in microglia and this upregulation could at least be attributed to JAK-STAT signaling pathway activated by IFN-γ and IL-10, which were spatio-temporally enriched in I/R injured brain as well...
September 13, 2017: Neuroscience
https://www.readbyqxmd.com/read/28916471/the-pyk2-mcu-pathway-in-the-rat-middle-cerebral-artery-occlusion-model-of-ischemic-stroke
#4
Kun Zhang, Jiajia Yan, Liang Wang, Xinying Tian, Tong Zhang, Li Guo, Bin Li, Wang Wang, Xiaoyun Liu
Mitochondrial dysfunction caused by Ca(2+) overload plays an important role in ischemia-induced brain damage. Mitochondrial calcium uniporter (MCU), located on the mitochondrial inner membrane, is the major channel responsible for mitochondrial Ca(2+) uptake. Activated proline-rich tyrosine kinase 2 (Pyk2) can directly phosphorylate MCU, which enhances mitochondrial Ca(2+) uptake in cardiomyocytes. It has been suggested that the Pyk2/MCU pathway may be a novel therapeutic target in stress-induced cellular apoptosis...
September 12, 2017: Neuroscience Research
https://www.readbyqxmd.com/read/28912644/tlr5-activation-through-nf-%C3%AE%C2%BAb-is-a-neuroprotective-mechanism-of-postconditioning-after-cerebral-ischemia-in-mice
#5
Jaewon Jeong, Soojin Kim, Da-Sol Lim, Seo-Hea Kim, Heeju Doh, So-Dam Kim, Yun Seon Song
Postconditioning has been shown to protect the mouse brain from ischemic injury. However, the neuroprotective mechanisms of postconditioning remain elusive. We have found that toll-like receptor 5 (TLR5) plays an integral role in postconditioning-induced neuroprotection through Akt/nuclear factor kappa B (NF-κB) activation in cerebral ischemia. Compared to animals that received 30 min of transient middle cerebral artery occlusion (tMCAO) group, animals that also underwent postconditioning showed a significant reduction of up to 60...
August 2017: Experimental Neurobiology
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
#6
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/28900508/direct-macromolecular-drug-delivery-to-cerebral-ischemia-area-using-neutrophil-mediated-nanoparticles
#7
Chun Zhang, Cheng-Li Ling, Liang Pang, Qi Wang, Jing-Xin Liu, Bing-Shan Wang, Jian-Ming Liang, Yi-Zhen Guo, Jing Qin, Jian-Xin Wang
Delivery of macromolecular drugs to the brain is impeded by the blood brain barrier. The recruitment of leukocytes to lesions in the brain, a typical feature of neuroinflammation response which occurs in cerebral ischemia, offers a unique opportunity to deliver drugs to inflammation sites in the brain. In the present study, cross-linked dendrigraft poly-L-lysine (DGL) nanoparticles containing cis-aconitic anhydride-modified catalase and modified with PGP, an endogenous tripeptide that acts as a ligand with high affinity to neutrophils, were developed to form the cl PGP-PEG-DGL/CAT-Aco system...
2017: Theranostics
https://www.readbyqxmd.com/read/28888980/arctigenin-attenuates-ischemic-stroke-via-sirt1-dependent-inhibition-of-nlrp3-inflammasome
#8
Shimeng Zhang, Liangjun Jiang, Fengyuan Che, Yucheng Lu, Zhongxiang Xie, Hao Wang
Arctigenin (ARC), a phenylpropanoid dibenzylbutyrolactone lignan derived from Arctium lappa L, has been reported to protect against cerebral ischemia injury in rats, but the underlying mechanism is unclear. In this study, we investigated whether ARC ameliorated ischemic stroke by inhibiting NLRP3 inflammasome-derived neuroinflammation and whether SIRT1 signaling was involved in this process. ARC (20 mg/kg) or vehicle were intraperitoneally injected to Sprague-Dawley rats for 3 days before middle cerebral artery occlusion (MCAO) surgery performed...
September 6, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28886009/tau-mediated-iron-export-prevents-ferroptotic-damage-after-ischemic-stroke
#9
Q-Z Tuo, P Lei, K A Jackman, X-L Li, H Xiong, X-L Li, Z-Y Liuyang, L Roisman, S-T Zhang, S Ayton, Q Wang, P J Crouch, K Ganio, X-C Wang, L Pei, P A Adlard, Y-M Lu, R Cappai, J-Z Wang, R Liu, A I Bush
Functional failure of tau contributes to age-dependent, iron-mediated neurotoxicity, and as iron accumulates in ischemic stroke tissue, we hypothesized that tau failure may exaggerate ischemia-reperfusion-related toxicity. Indeed, unilateral, transient middle cerebral artery occlusion (MCAO) suppressed hemispheric tau and increased iron levels in young (3-month-old) mice and rats. Wild-type mice were protected by iron-targeted interventions: ceruloplasmin and amyloid precursor protein ectodomain, as well as ferroptosis inhibitors...
September 8, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28883752/rhglp-1-7-36-protects-diabetic-rats-against-cerebral-ischemia-reperfusion-injury-via-up-regulating-expression-of-nrf2-ho-1-and-increasing-the-activities-of-sod
#10
Yi Fang, Xiaofang Liu, Libo Zhao, Zhongna Wei, Daoli Jiang, Hua Shao, Yannan Zang, Jia Xu, Qian Wang, Yang Liu, Ye Peng, Xiaoxing Yin
The present study aimed to explore the neuroprotective effect and possible mechanisms of rhGLP-1 (7-36) against transient ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in type 2 diabetic rats. First, diabetic rats were established by a combination of a high-fat diet and low-dose streptozotocin (STZ) (30 mg/kg, intraperitoneally). Second, they were subjected to MCAO for 2 h, then treated with rhGLP-1 (7-36) (10, 20, 40 µg/kg i.p.) at the same time of reperfusion. In the following 3 days, they were injected with rhGLP-1 (7-36) at the same dose and route for three times each day...
September 2017: Korean Journal of Physiology & Pharmacology
https://www.readbyqxmd.com/read/28876976/trpm4-activation-by-chemically-and-oxygen-deprivation-induced-ischemia-and-reperfusion-triggers-neuronal-death
#11
Elías Leiva-Salcedo, Denise Riquelme, Oscar Cerda, Andrés Stutzin
Cerebral ischemia-reperfusion injury triggers a deleterious process ending in neuronal death. This process has two components, a glutamate-dependent and a glutamate-independent mechanism. In the glutamate-independent mechanism, neurons undergo a slow depolarization eventually leading to neuronal death. However, little is known about the molecules that take part in this process. Here we show by using mice cortical neurons in culture and ischemia-reperfusion protocols that TRPM4 is fundamental for the glutamate-independent neuronal damage...
September 6, 2017: Channels
https://www.readbyqxmd.com/read/28876179/the-inhibitory-effects-of-dracocephalum-moldavica-l-dml-on-rat-cerebral-ischemia-reperfusion-injury
#12
Jian-Xin Jia, Yu Zhang, Zhan-Li Wang, Xu-Sheng Yan, Min Jin, Dong-Sheng Huo, He Wang, Zhan-Jun Yang
Ischemia reperfusion injury (IRI) is closely associated with oxidative stress and inflammatory responses. Dracocephalum moldavica L. (DML), a Chinese herbal medicine is known to exert protective effects on myocardial ischemia reperfusion injury in rats by inhibiting oxidation damage and inflammatory reactions. However, the effectiveness of DML in cerebral ischemia reperfusion injury (CIRI) as a protective substance and the underlying mechanisms remain to be determined. The aim of this study was thus to examine the influence of DML on CIRI using a rat model induced by 2-h transient middle cerebral artery occlusion (MCAO) produced by intraluminal suture blockade followed by 22 h reperfusion...
September 6, 2017: Journal of Toxicology and Environmental Health. Part A
https://www.readbyqxmd.com/read/28874782/dihydrocapsaicin-attenuates-blood-brain-barrier-and-cerebral-damage-in-focal-cerebral-ischemia-reperfusion-via-oxidative-stress-and-inflammatory
#13
Adchara Janyou, Piyawadee Wicha, Jinatta Jittiwat, Apichart Suksamrarn, Chainarong Tocharus, Jiraporn Tocharus
This study investigated the effect of dihydrocapsaicin (DHC) on cerebral and blood brain barrier (BBB) damage in cerebral ischemia and reperfusion (I/R) models. The models were induced by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion. The rats were divided into five groups: sham, or control group; vehicle group; and 2.5 mg/kg, 5 mg/kg, and 10 mg/kg BW DHC-treated I/R groups. After 24 h of reperfusion, we found that DHC significantly reduced the area of infarction, morphology changes in the neuronal cells including apoptotic cell death, and also decreased the BBB damage via reducing Evan Blue leakage, water content, and ultrastructure changes, in addition to increasing the tight junction (TJ) protein expression...
September 5, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28871473/role-of-peroxiredoxin-2-in-the-protection-against-ferrous-sulfate-induced-oxidative-and-inflammatory-injury-in-pc12-cells
#14
Wenzhe Xu, Feng Li, Zhenkuan Xu, Bin Sun, Jingwei Cao, Yuguang Liu
Peroxiredoxin 2 (Prdx2) is a ubiquitous antioxidant enzyme in mammalian brain. Although a protective role of Prdx2 has been established in cerebral ischemia and several neurodegenerative diseases, its contribution against iron-induced neurocytotoxicity still remains to be determined. Accordingly, in this study, we aimed to investigate the effects of Prdx2 on iron-induced cytotoxicity using an in vitro model in which PC12 cells are exposed to ferrous sulfate (FS). The FS treatment increased Prdx2 expression, and promoted lactate dehydrogenase (LDH) release and cell apoptosis in PC12 cells, accompanied by the increase in the Bax/Bcl2 ratio, cytochrome c release, and caspase-3 cleavage...
September 4, 2017: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/28865993/genetic-neutrophil-deficiency-ameliorates-cerebral-ischemia-reperfusion-injury
#15
Ryan A Frieler, Yutein Chung, Carolyn G Ahlers, George Gheordunescu, Jianrui Song, Thomas M Vigil, Yatrik M Shah, Richard M Mortensen
Neutrophils respond rapidly to cerebral ischemia and are thought to contribute to inflammation-mediated injury during stroke. Using myeloid Mcl1 knockout mice as a model of genetic neutrophil deficiency, we investigated the contribution of neutrophils to stroke pathophysiology. Myeloid Mcl1 knockout mice were subjected to transient middle cerebral artery occlusion and infarct size was assessed by MRI after 24h reperfusion. Immune cell mobilization and infiltration was assessed by flow cytometry. We found that myeloid Mcl1 knockout mice had significantly reduced infarct size when compared to heterozygous and wild type control mice (MyMcl1(+/+): 78...
August 31, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28854873/effects-and-mechanism-of-dexmedetomidine-on-neuronal-cell-injury-induced-by-hypoxia-ischemia
#16
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/28854286/therapeutic-time-window-for-conivaptan-treatment-against-stroke-evoked-brain-edema-and-blood-brain-barrier-disruption-in-mice
#17
Emil Zeynalov, Susan M Jones, J Paul Elliott
BACKGROUND: Ischemic stroke is often complicated by brain edema, disruption of blood-brain barrier (BBB), and uncontrolled release of arginine-vasopressin (AVP). Conivaptan, a V1a and V2 receptor antagonist, reduces brain edema and minimizes damage to the blood-brain barrier after stroke. Most stroke patients do not receive treatment immediately after the onset of brain ischemia. Delays in therapy initiation may worsen stroke outcomes. Therefore, we designed a translational study to explore the therapeutic time window for conivaptan administration...
2017: PloS One
https://www.readbyqxmd.com/read/28852468/phosphorylation-of-astrocytic-connexin43-by-erk1-2-impairs-blood-brain-barrier-in-acute-cerebral-ischemia
#18
Wei Chen, Jiugeng Feng, Wusong Tong
BACKGROUND: Connexins are a family of transmembrane proteins that form gap junctions, which are important for diffusion of cytosolic factors such as ions and second messenger signaling molecules. Our previous study has shown that Connexin40 (Cx40), one dominant connexin expressed in brain, was involved in brain injury. In this study, Cx43, another dominant connexin in brain, was investigated. Using bilateral common carotid artery occlusion-induced ischemia rat model, we tested the expression and phosphorylation level of Cx43 as well as heteromeric Cx40/Cx43 complex formation in brain after ischemia induction...
2017: Cell & Bioscience
https://www.readbyqxmd.com/read/28851669/nrf2-inhibits-nlrp3-inflammasome-activation-through-regulating-trx1-txnip-complex-in-cerebral-ischemia-reperfusion-injury
#19
Yanghao Hou, Yueting Wang, Qi He, Lingyu Li, Hui Xie, Yong Zhao, Jing Zhao
The nod-like receptor protein 3 (NLRP3) inflammasome has a critical role in inflammation damage in ischemic injury, and the activation of the inflammasome is closely related to the interaction with thioredoxin interacting protein (TXNIP), which dissociates from the thioredoxin1 (Trx1)/TXNIP complex under oxidative stress. However, the negative regulator of NLRP3 inflammasome activation has not been fully investigated. Nuclear factor erythroid 2-related factor 2 (Nrf2) takes on a critical part in the antioxidant stress system, that controls the driven genes of antioxidant response element (ARE)...
August 26, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28844957/adiponectin-attenuates-nadph-oxidase-mediated-oxidative-stress-and-neuronal-damage-induced-by-cerebral-ischemia-reperfusion-injury
#20
Xia Li, Hao Guo, Lei Zhao, Bodong Wang, Haixiao Liu, Liang Yue, Hao Bai, Haiyang Jiang, Li Gao, Dayun Feng, Yan Qu
Adiponectin (APN), which is a major adipokine that regulated glucose and lipid metabolism, plays an important role in the protection of the cerebral nervous system. It also has been suggested to have anti-inflammatory effects and ameliorate oxidative stress. Stroke is a universal cause of death and permanent disability. Ischemic stroke accounts for most cases of stroke, and is characterized by cerebral ischemia and neurological deficits. We aimed to investigate the effects of APN-peptide (APN-P) in neurons following ischemia reperfusion (I/R) in C57BL/6J mice, and to study the potential mechanisms underlying its effects...
August 24, 2017: Biochimica et Biophysica Acta
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