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Condition: Hemorrhagic Stroke

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Total 120 results found since Jan 2013.

SOCS and Herpesviruses, With Emphasis on Cytomegalovirus Retinitis
Christine I. Alston1,2 and Richard D. Dix1,2* 1Department of Biology, Viral Immunology Center, Georgia State University, Atlanta, GA, United States 2Department of Ophthalmology, Emory University School of Medicine, Atlanta, GA, United States Suppressor of cytokine signaling (SOCS) proteins provide selective negative feedback to prevent pathogeneses caused by overstimulation of the immune system. Of the eight known SOCS proteins, SOCS1 and SOCS3 are the best studied, and systemic deletion of either gene causes early lethality in mice. Many viruses, including herpesviruses such as herpes simplex virus and cytomega...
Source: Frontiers in Immunology - April 10, 2019 Category: Allergy & Immunology Source Type: research

Apelin-13 attenuates early brain injury following subarachnoid hemorrhage via suppressing neuronal apoptosis through the GLP-1R/PI3K/Akt signaling.
Abstract Apelin, an endogenous ligand for the orphan G-protein-coupled receptor APJ, possesses anti-apoptotic and neuroprotective properties. It has been shown to be a protective factor for different types of central nervous system insults, such as ischemia and traumatic brain injury. Here, we investigated the effects of apelin-13 on early brain injury (EBI) following subarachnoid hemorrhage (SAH), and the underlying molecular mechanisms involved. Apelin-13 was delivered to rats via intracerebroventricular administration. Neurological scores, brain water content and neuronal apoptosis were measured 24 h after SA...
Source: Biochemical and Biophysical Research communications - March 28, 2019 Category: Biochemistry Authors: Liu Y, Zhang T, Wang Y, Wu P, Li Y, Wang C, Xu S, Shi H Tags: Biochem Biophys Res Commun Source Type: research

Apc gene suppresses intracranial aneurysm formation and rupture through inhibiting the NF- κB signaling pathway mediated inflammatory response.
CONCLUSION: All above, Apc has the potential role to attenuate IA formation and rupture by inhibiting inflammatory response through repressing the activation of the NF-κB signaling pathway. PMID: 30808715 [PubMed - as supplied by publisher]
Source: Bioscience Reports - February 26, 2019 Category: Biomedical Science Authors: Lai XL, Deng ZF, Zhu XG, Chen ZH Tags: Biosci Rep Source Type: research

Mitoquinone attenuates blood-brain barrier disruption through Nrf2/PHB2/OPA1 pathway after subarachnoid hemorrhage in rats.
CONCLUSIONS: MitoQ attenuates blood-brain barrier disruption via Nrf2/PHB2/OPA1 pathway after SAH in rats. MitoQ may serve as a potential therapeutic strategy for SAH patients. PMID: 30779914 [PubMed - as supplied by publisher]
Source: Experimental Neurology - February 16, 2019 Category: Neurology Authors: Zhang T, Xu S, Wu P, Zhou K, Wu L, Xie Z, Xu W, Luo X, Li P, Ocak U, Ocak PE, Travis ZD, Tang J, Shi H, Zhang JH Tags: Exp Neurol Source Type: research

Tristetraprolin attenuates brain edema in a rat model of cerebral hemorrhage
ConclusionTaken together, these data indicate that TTP has a protective role against brain edema by reducing inflammation, apoptosis, and water content in the brain at 48  hr after cerebral hemorrhage. Our findings may be useful for developing important approaches to treating brain injury.
Source: Brain and Behavior - February 6, 2019 Category: Neurology Authors: Peiyu Li, Junwu Zhang, Xin Li, Hongwei Gao Tags: ORIGINAL RESEARCH Source Type: research

Inhibition of BECN1 Suppresses Lipid Peroxidation by Increasing System X c − Activity in Early Brain Injury after Subarachnoid Hemorrhage
This study confirmed that SAH induced neurological deficits and brain edema, which was accompanied by the increase of BECN1 expression and lipid peroxidation, and the decrease of xCT expression and antioxidative capacity. However, downregulation of BECN1 by siRNA could decrease the formation of the BECN1 –xCT complex and lipid peroxidation, enhance antioxidative capacity, and ameliorate neurological deficits and brain edema in SAH rats. The results suggested that inhibition of BECN1 suppresses accumulation of lipid peroxidation by increasing system Xc− activity in EBI after SAH, and BECN1 may be a new effective target ...
Source: Journal of Molecular Neuroscience - February 4, 2019 Category: Neuroscience Source Type: research

rh-IFN-α Attenuates Neuroinflammation and Improves Neurological Function by Inhibiting NF-κB through JAK1-STAT1/TRAF3 Pathway in an Experimental GMH Rat Model
In conclusion, our findings demonstrated that rh-IFN-α treatment attenuated neuroinflammation, neurological deficits and hydrocephalus formation through inhibiting microglial activation after GMH, which might be mediated by IFNAR/JAK1-STAT1/TRAF3/NF-κB signaling pathway. Rh-IFN-α may be a promising therapeutic agent to attenuate brain injury via its anti-inflammatory effect.
Source: Brain, Behavior, and Immunity - February 1, 2019 Category: Neurology Source Type: research

Annexin A7 induction of neuronal apoptosis via effect on glutamate release in a rat model of subarachnoid hemorrhage.
CONCLUSIONSANXA7 can induce neuronal apoptosis by affecting glutamate release in rats with SAH. Downregulating the expression of ANXA7 can significantly attenuate early brain injury after SAH. Future therapy targeting ANXA7 may be a promising new choice. PMID: 30717037 [PubMed - as supplied by publisher]
Source: Journal of Neurosurgery - February 1, 2019 Category: Neurosurgery Authors: Lin QS, Wang WX, Lin YX, Lin ZY, Yu LH, Kang Y, Kang DZ Tags: J Neurosurg Source Type: research

GATA-4 regulates neuronal apoptosis after intracerebral hemorrhage via the NF- κB/Bax/Caspase-3 pathway both in vivo and in vitro.
In conclusion, the expression of GATA-4 was increased in the brain of rats after ICH. GATA-4 phosphorylation mediates the function of the protein in ICH-induced SBI. Neuronal apoptosis after ICH was mainly induced by NF-κB activation, which was promoted by GATA-4. PMID: 30710529 [PubMed - as supplied by publisher]
Source: Experimental Neurology - January 30, 2019 Category: Neurology Authors: Xu H, Cao J, Xu J, Li H, Shen H, Li X, Wang Z, Wu J, Chen G Tags: Exp Neurol Source Type: research

LRP1 activation attenuates white matter injury by modulating microglial polarization through Shc1/PI3K/Akt pathway after subarachnoid hemorrhage in rats
Publication date: Available online 23 January 2019Source: Redox BiologyAuthor(s): Jianhua Peng, Jinwei Pang, Lei Huang, Budbazar Enkhjargal, Tongyu Zhang, Jun Mo, Pei Wu, Weilin Xu, Yuchun Zuo, Jun Peng, Gang Zuo, Ligang Chen, Jiping Tang, John H. Zhang, Yong JiangAbstractWhite matter injury (WMI) is associated with motor deficits and cognitive dysfunctions in subarachnoid hemorrhage (SAH) patients. Therapeutic strategy targeting WMI would likely improve the neurological outcomes after SAH. Low-density lipoprotein receptor-related protein-1 (LRP1), a scavenger receptor of apolipoprotein E (apoE), is able to modulate microg...
Source: Redox Biology - January 24, 2019 Category: Biology Source Type: research

Administration of rCTRP9 Attenuates Neuronal Apoptosis Through AdipoR1/PI3K/Akt Signaling Pathway after ICH in Mice.
Abstract Targeting neuronal apoptosis after intracerebral hemorrhage (ICH) may be an important therapeutic strategy for ICH patients. Emerging evidence indicates that C1q/TNF-Related Protein 9 (CTRP9), a newly discovered adiponectin receptor agonist, exerts neuroprotection in cerebrovascular disease. The aim of this study was to investigate the anti-apoptotic role of CTRP9 after experimental ICH and to explore the underlying molecular mechanisms. ICH was induced in mice via intrastriatal injection of bacterial collagenase. Recombinant CTRP9 (rCTRP9) was administrated intranasally at 1 h after ICH. To elucidate the...
Source: Cell Transplantation - January 14, 2019 Category: Cytology Authors: Zhao L, Zhang JH, Sherchan P, Krafft PR, Zhao W, Wang S, Chen S, Guo Z, Tang J Tags: Cell Transplant Source Type: research

Macrophage stimulating protein preserves blood brain barrier integrity after intracerebral hemorrhage through recepteur d'origine nantais dependent GAB1/Src/ β‐catenin pathway activation in a mouse model
This study aimed to evaluate the role of MSP and RON activated signaling pathway in preserving BBB integrity after collagenase‐induced ICH. ICH mice received recombinant human MSP (rhMSP) or rhMSP combined with siRNA knockdown of RON or GAB1. rhMSP was administered by intranasal route 1 h after ICH. Brain edema, neurobehavior, BBB tight junction protein exp ression, and BBB permeability were evaluated. The expression of endogenous MSP and p‐RON was decreased after ICH. Exogenous rhMSP administration reduced brain edema, neurological deficits, BBB permeability, and increased the expression of tight junction proteins in...
Source: Journal of Neurochemistry - December 5, 2018 Category: Neuroscience Authors: Tai Lu, Zhong Wang, Sherchan Prativa, Yang Xu, Tian Wang, Yiting Zhang, Lingyan Yu, Ningbo Xu, Jiping Tang, Wanchun You, Gang Chen, John H. Zhang Tags: Original Article Source Type: research

Aquaporins in brain edema
Following brain injury, the astrocyte water channel AQP4 mediates edema formation and resolution. Several factors modulate the actions of AQP4 including: (a) AQP4 membrane distribution into arrays, depending on the ratio of AQP4 isoforms; (b) AQP4 interactions with ion channels and gap junctions; (c) temporal variations in AQP4 expression. AbstractBrain edema is a common feature of brain injuries, which leads to increased intracranial pressure (ICP) and ischemia that worsen outcome. Current management of edema focuses on reduction of ICP, but there are no treatments targeting the molecular players directly involved in edem...
Source: Journal of Neuroscience Research - November 15, 2018 Category: Neuroscience Authors: Tifenn Cl ément, Beatriz Rodriguez‐Grande, Jérôme Badaut Tags: REVIEW Source Type: research

AVE 0991 attenuates oxidative stress and neuronal apoptosis via Mas/PKA/CREB/UCP-2 pathway after subarachnoid hemorrhage in rats
In conclusion, our data provides evidence that Mas activation with AVE reduces oxidative stress injury and neuronal apoptosis through Mas/PKA/p-CREB/UCP-2 pathway after SAH. Furthermore, our study indicates that Mas may be a novel therapeutic treatment target in early brain injury of SAH.Graphical abstract
Source: Redox Biology - October 5, 2018 Category: Biology Source Type: research