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Condition: Hemorrhagic Stroke

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Total 120 results found since Jan 2013.

IGF-1R stimulation alters microglial polarization via TLR4/NF- κB pathway after cerebral hemorrhage in mice.
In this study, we examined the impact of insulin-like growth factor-1 (IGF-1) secreted by NSCs on microglial polarization following ICH in adult C57BL/6 mice. Mouse models of ICH were established by collagenase injection. ICH mice received NSC transplantation after one hour. Firstly, the changes of microglial polarization in cerebral tissues of ICH mice were detected by immunofluorescence and ELISA. Secondly, the molecular mechanism underlying the microglial polarization was evaluated repeatedly with the application of IGF-1R siRNA and IGF-1R-mediated inhibition. We assessed the brain water content and behavioral deficits ...
Source: Brain Research Bulletin - August 28, 2020 Category: Neurology Authors: Sun Z, Wu K, Gu L, Huang L, Zhuge Q, Yang S, Wang Z Tags: Brain Res Bull Source Type: research

Targeting CCL20 inhibits subarachnoid hemorrhage-related neuroinflammation in mice.
Abstract Recent evidence suggests that CC chemokine ligand 20 (CCL20) is upregulated after subarachnoid hemorrhage (SAH). Here, we investigated the functions of CCL20 in SAH injury and its underlying mechanisms of action. We found that CCL20 is upregulated in an SAH mouse model and in cultured primary microglia and neurons. CCL20-neutralizing antibody alleviated SAH-induced neurological deficits, decreased brain water content and neuronal apoptosis, and repressed microglial activation. We observed increased levels of CCL20, CC chemokine receptor 6 (CCR6), interleukin 1 beta (IL-1β), and tumor necrosis factor alph...
Source: Aging - June 20, 2020 Category: Biomedical Science Authors: Liao LS, Zhang MW, Gu YJ, Sun XC Tags: Aging (Albany NY) Source Type: research

HLY78 protects blood-brain barrier integrity through Wnt/ β-catenin signaling pathway following subarachnoid hemorrhage in rats.
In conclusion, HLY78 could preserve BBB integrity, possibly through the Wnt/β-catenin signaling pathway. HLY78 might be a potential treatment option to protect BBB integrity following SAH. PMID: 32565130 [PubMed - as supplied by publisher]
Source: Brain Research Bulletin - June 17, 2020 Category: Neurology Authors: Luo X, Li L, Zheng W, Gu L, Zhang X, Li Y, Xie Z, Cheng Y Tags: Brain Res Bull Source Type: research

Occludin degradation makes brain microvascular endothelial cells more vulnerable to reperfusion injury in vitro
AbstractIntracerebral hemorrhage is the most dangerous complication in tPA thrombolytic therapy for ischemic stroke, which occurs as a consequence of endothelial cell death at the blood brain barrier (BBB) during thrombolytic reperfusion. We have previously shown that cerebral ischemia induced rapid occludin degradation and BBB disruption. Here we demonstrated an important role of occludin degradation in facilitating the evolution of ischemic endothelial cells towards death. Cultured brain microvascular endothelial cells (bEnd.3 cells) were exposed to oxygen ‐glucose deprivation (OGD) or incubated with occludin siRNA or ...
Source: Journal of Neurochemistry - June 11, 2020 Category: Neuroscience Authors: Yuan Zhang, Xiaofeng Li, Shanshan Qiao, Dexin Yang, Zongyang Li, Ji Xu, Weiping Li, Li Su, Wenlan Liu Tags: ORIGINAL ARTICLE Source Type: research

lncRNA Mtss1 promotes inflammatory responses and secondary brain injury after intracerebral hemorrhage by targeting miR-709 in mice.
Abstract Secondary brain injuries following intracerebral hemorrhage (ICH) are mediated by inflammatory pathway activation. The present study aimed to characterize long noncoding RNAs (lncRNAs) that are differentially expressed in cerebral tissues during ICH pathogenesis and to investigate their pathogenic functions. An ICH mouse model established by collagenase injection was used to obtain differentially expressed lncRNAs for deep sequencing. A cellular inflammation model was established by treating mouse microglia with lipopolysaccharide. Expression of lncRNA and miRNA was assessed by quantitative RT-PCR, and pr...
Source: Brain Research Bulletin - May 18, 2020 Category: Neurology Authors: Chen JX, Wang YP, Zhang X, Li GX, Zheng K, Duan CZ Tags: Brain Res Bull Source Type: research

Recombinant OX40 attenuates neuronal apoptosis through OX40-OX40L/PI3K/AKT signaling pathway following subarachnoid hemorrhage in rats.
Abstract Subarachnoid hemorrhage (SAH) is the most devastating form of stroke. Reducing neuronal apoptosis is an important countermeasure against early brain injury (EBI) after SAH. Recent evidence indicates that OX40-OX40L coupling is critical for cell survival and proliferation. Current study was performed to detect the role of recombinant OX40 (ReOX40) against neuronal apoptosis after SAH. The endovascular perforation model of SAH was performed on Sprague-Dawley (SD) rats. ReOX40 was injected intracerebroventricularly (i.c.v) 1 h after SAH induction and the following methods were employed: neurological functi...
Source: Experimental Neurology - January 9, 2020 Category: Neurology Authors: Wu LY, Enkhjargal B, Xie ZY, Travis ZD, Sun CM, Zhou KR, Zhang TY, Zhu QQ, Hang CH, Zhang JH Tags: Exp Neurol Source Type: research

Intranasal wnt-3a alleviates neuronal apoptosis in early brain injury post subarachnoid hemorrhage via the regulation of wnt target PPAN mediated by the moonlighting role of aldolase C
Publication date: Available online 31 December 2019Source: Neurochemistry InternationalAuthor(s): Wu Ruan, Junwen Hu, Hang Zhou, Yin Li, Chaoran Xu, Yujie Luo, Ting Chen, Bangliang Xu, Feng Yan, Gao ChenAbstractNeuronal apoptosis is one of the main pathophysiological events in the early brain injury (EBI) post subarachnoid hemorrhage (SAH). Wnt-3a, one of the endogenous wnt ligands crucial in neurogenesis, has been proven to be efficacious in neuroprotection in traumatic brain injury and ischemic stroke. The glycolytic enzyme aldolase C and ribosome biogenesis protein PPAN were revealed to be linked to wnt signaling pathwa...
Source: Neurochemistry International - January 1, 2020 Category: Neuroscience Source Type: research

Elastin-derived peptide VGVAPG affects the proliferation of mouse cortical astrocytes with the involvement of aryl hydrocarbon receptor (Ahr), peroxisome proliferator-activated receptor gamma (Ppar γ), and elastin-binding protein (EBP).
Elastin-derived peptide VGVAPG affects the proliferation of mouse cortical astrocytes with the involvement of aryl hydrocarbon receptor (Ahr), peroxisome proliferator-activated receptor gamma (Pparγ), and elastin-binding protein (EBP). Cytokine. 2019 Nov 21;126:154930 Authors: Szychowski KA, Gmiński J Abstract During aging and ischemic and hemorrhagic stroke, elastin molecules are degraded and elastin-derived peptides are released into the brain microenvironment. Val-Gly-Val-Ala-Pro-Gly (VGVAPG) is a repeating hexapeptide in the elastin molecule. It is well documented that the peptide sequence binds...
Source: Cytokine - November 20, 2019 Category: Molecular Biology Authors: Szychowski KA, Gmiński J Tags: Cytokine Source Type: research

LncRNA Snhg3 contributes to dysfunction of cerebral microvascular cells in intracerebral hemorrhage rats by activating the TWEAK/Fn14/STAT3 pathway
In conclusion, the lncRNA Snhg3 contributes to dysfunction of cerebral microvascular cells in ICH rats by activating the TWEAK/Fn14/STAT3 pathway.
Source: Life Sciences - October 11, 2019 Category: Biology Source Type: research

Eupatilin attenuates the inflammatory response induced by intracerebral hemorrhage through the TLR4/MyD88 pathway.
CONCLUSION: Eupatilin has a therapeutic effect on inflammation caused by ICH. The underlying mechanism may be related to TLR4/MyD88, which brings new hope for clinical patients to improve symptoms and prognosis. PMID: 31476693 [PubMed - as supplied by publisher]
Source: International Immunopharmacology - August 29, 2019 Category: Allergy & Immunology Authors: Fei X, Chen C, Kai S, Fu X, Man W, Ding B, Wang C, Xu R Tags: Int Immunopharmacol Source Type: research

Delayed recanalization at 3 days after permanent MCAO attenuates neuronal apoptosis through FGF21/FGFR1/PI3K/Caspase-3 pathway in rats.
Abstract Reperfusion exceeded time window may induce ischemia/reperfusion injury, increase hemorrhagic transformation, and deteriorate neurological outcomes in ischemic stroke models. However, the increasing clinical evidences supported that reperfusion even within 6-24 h may salvage ischemic tissue and improve neurological outcomes in selected large vessel occlusion patients, without inducing serious ischemia/reperfusion injury and hemorrhagic transformation. The underlying molecular mechanisms are less clear. In present study, we demonstrated that delayed recanalization at 3 days after permanent middle cereb...
Source: Experimental Neurology - July 7, 2019 Category: Neurology Authors: Zheng W, Matei N, Pang J, Luo X, Song Z, Tang J, Zhang JH Tags: Exp Neurol Source Type: research

Activation of GPR30 with G1 attenuates neuronal apoptosis via src/EGFR/stat3 signaling pathway after subarachnoid hemorrhage in male rats.
CONCLUSION: G1 reduced EBI through attenuating neuronal apoptosis after SAH in male rats, partly via activating src/EGFR/stat3/signaling pathway. G1 may provide a promising therapeutic strategy for SAH patients. PMID: 31295444 [PubMed - as supplied by publisher]
Source: Experimental Neurology - July 7, 2019 Category: Neurology Authors: Peng J, Zuo Y, Huang L, Okada T, Liu S, Zuo G, Zhang G, Tang J, Xia Y, Zhang JH Tags: Exp Neurol Source Type: research

FGF-2 Attenuates Neuronal Apoptosis via FGFR3/PI3k/Akt Signaling Pathway After Subarachnoid Hemorrhage
AbstractNeuronal apoptosis is a common and critical pathology following subarachnoid hemorrhage (SAH). We investigated the anti-apoptotic property of fibroblast growth factor (FGF)-2 after SAH in rats. A total of 289 rats underwent endovascular perforation to induce SAH or sham operation. Three dosages (3, 9, or 27  μg) of recombinant FGF-2 (rFGF-2) or vehicle was administered intranasally to rats 30 min after SAH induction. The pan-FGF receptor (FGFR) inhibitor PD173074 or vehicle was administered intracerebroventricularly (i.c.v.) 1 h before modeling, in addition to rFGF-2 treatment. Small interfering ri bonucleic ac...
Source: Molecular Neurobiology - June 14, 2019 Category: Neurology Source Type: research

AdipoRon attenuates neuroinflammation after intracerebral hemorrhage through AdipoR1-AMPK pathway
Publication date: Available online 7 June 2019Source: NeuroscienceAuthor(s): Jingwei Zheng, Zeyu Sun, Feng Liang, Weilin Xu, Jianan Lu, Ligen Shi, Anwen Shao, Jun Yu, Jianmin ZhangAbstractNeuroinflammation is considered to be a critical component in the pathological process after intracerebral hemorrhage (ICH). Microglia are the foremost and earliest inflammatory cells participating in the pathological process of ICH. AdipoRon is the agonist of AdipoR1 (Adiponectin receptor 1), which enhances P-AMPK (phosphorylated AMP-activated protein kinase) activation. The activated AMPK facilitates microglia/macrophage polarization by...
Source: Neuroscience - June 7, 2019 Category: Neuroscience Source Type: research

Naringenin Produces Neuroprotection Against LPS-Induced Dopamine Neurotoxicity via the Inhibition of Microglial NLRP3 Inflammasome Activation
Conclusions: This study demonstrated that NAR targeted microglial NLRP3 inflammasome to protect DA neurons against LPS-induced neurotoxicity. These findings suggest NAR might hold a promising therapeutic potential for PD. Background Parkinson's disease (PD) is the second most prevalent central nervous system (CNS) degenerative disease. It is characterized by slow and progressive loss of dopamine (DA) neurons in the midbrain substantia nigra (SN) with the accumulation of α-synuclein in Lewy bodies and neuritis (1). Although the etiology of PD remains unclear, amounts of studies have suggested that ne...
Source: Frontiers in Immunology - April 30, 2019 Category: Allergy & Immunology Source Type: research