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Condition: Hemorrhagic Stroke
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Total 120 results found since Jan 2013.
Silencing of ATM expression by siRNA technique contributes to glioma stem cell radiosensitivity in vitro and in vivo.
In conclusion, silencing of ATM via the siRNA technique improved radiosensitivity of GSCs both in vitro and in vivo.
PMID: 28560406 [PubMed - as supplied by publisher]
Source: Oncology Reports - June 2, 2017 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research
TRAF6 participates in early brain injury after subarachnoid hemorrhage in rats through inhibiting autophagy and promoting oxidative stress
This study was designed to explore changes of expression level and potential roles and mechanisms of TRAF6 in early brain injury (EBI) after SAH by using a Sprague–Dawley rat model of SAH induced in 0.3 ml non‐heparinized autologous arterial blood injected into the prechiasmatic cistern. First, compared with the sham group, we found that the expression levels of TRAF6 increased gradually and peaked at 24 h after SAH. Second, the results showed that application of TRAF6 overexpression plasmid and genetic silencing siRNA could increase or decrease expression of TRAF6, respectively, and severely exacerbate or relieve EBI ...
Source: Journal of Neurochemistry - May 24, 2017 Category: Neurology Authors: Yang Dou, Haitao Shen, Dongxia Feng, Haiying Li, Xiaodi Tian, Jian Zhang, Zhong Wang, Gang Chen Tags: Original Article Source Type: research
Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD+/Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats Basic Sciences
Conclusions—HBO induced activation of ATP/nicotinamide adenine dinucleotide/silent mating type information regulation 2 homolog 1 pathway and protected blood–brain barrier in hyperglycemic middle cerebral artery occlusion rats. HBO might be promising approach for treatment of acute ischemic stroke patients, especially patients with diabetes mellitus or treated with r-tPA (recombinant tissue-type plasminogen activator).
Source: Stroke - May 22, 2017 Category: Neurology Authors: Qin Hu, Anatol Manaenko, Hetao Bian, Zongduo Guo, Jun-Long Huang, Zhen-Ni Guo, Peng Yang, Jiping Tang, John H. Zhang Tags: Animal Models of Human Disease, Basic Science Research, Ischemia, Neuroprotectants Original Contributions Source Type: research
P2X7 Participates in Intracerebral Hemorrhage-Induced Secondary Brain Injury in Rats via MAPKs Signaling Pathways.
This study aimed to study the role of P2X7 in intracerebral hemorrhage (ICH)-induced secondary brain injury (SBI) and the underlying mechanisms. An autologous blood injection was used to induce ICH model in Sprague-Dawley rats, and cultured primary rat cortical neurons were exposed to oxyhemoglobin to mimic ICH in vitro. siRNA interference and over-expression of P2X7, agonists and antagonists of P2X7, p38 MAPK and ERK were exploited. The protein levels were assessed using Western blotting and immunofluorescence staining. Terminal deoxynucleotidyl transferase dUTP nick end labeling staining and Fluoro-Jade B were conducted ...
Source: Neurochemical Research - May 9, 2017 Category: Neuroscience Authors: Wen Z, Mei B, Li H, Dou Y, Tian X, Shen M, Chen G Tags: Neurochem Res Source Type: research
DLK silencing attenuated neuron apoptosis through JIP3/MA2K7/JNK pathway in early brain injury after SAH in rats.
CONCLUSIONS: As a negative role, DLK was involved in EBI after SAH, possibly mediated by its adaptor protein JIP3 and MA2K7/JNK signaling pathways. To reduce the level of DLK may be a new target as intervention for SAH.
PMID: 28396258 [PubMed - as supplied by publisher]
Source: Neurobiology of Disease - April 7, 2017 Category: Neurology Authors: Yin C, Huang GF, Sun XC, Guo Z, Zhang JH Tags: Neurobiol Dis Source Type: research
Involvement of Nox2 and Nox4 NADPH oxidases in early brain injury after subarachnoid hemorrhage.
In conclusion, Nox4 should contribute to the pathological processes in SAH-induced EBI, and there was not an overlay effect of Nox2 inhibition and Nox4 inhibition on preventing SAH-induced EBI.
PMID: 28330417 [PubMed - as supplied by publisher]
Source: Free Radical Research - March 24, 2017 Category: Research Tags: Free Radic Res Source Type: research
Intranasal administration of recombinant Netrin-1 attenuates neuronal apoptosis by activating DCC/APPL-1/AKT signaling pathway after subarachnoid hemorrhage in rats.
Abstract
Neuronal apoptosis is a crucial pathological process in early brain injury after subarachnoid hemorrhage (SAH). The effective therapeutic strategies to ameliorate neuronal apoptosis are still absent. We intended to determine whether intranasal administration of exogenous Netrin-1 (NTN-1) could attenuate neuronal apoptosis after experimental SAH, specifically via activating DCC-dependent APPL-1/AKT signaling cascade. Two hundred twenty-five male Sprague-Dawley rats were subjected to the endovascular perforation model of SAH. Recombinant human NTN-1 (rNTN-1) was administered intranasally. NTN-1 small interf...
Source: Neuropharmacology - March 24, 2017 Category: Drugs & Pharmacology Authors: Xie Z, Huang L, Enkhjargal B, Reis C, Wan W, Tang J, Cheng Y, Zhang JH Tags: Neuropharmacology Source Type: research
Artesunate Protected Blood –Brain Barrier via Sphingosine 1 Phosphate Receptor 1/Phosphatidylinositol 3 Kinase Pathway After Subarachnoid Hemorrhage in Rats
This study was designed to investigate the protective effect and mechanism of artesunate, a traditional anti-malaria drug, on blood–brain barrier after SAH. Three hundred and seventy-seven (377) male Sprague–Dawley rats were subjected to endovascular perforation model for SAH. The rats received artesunate alone or in combination with Sphingosine-1-phosphate receptor-1 (S1P1) small interfering RNA (siRNA), antagonist VPC23019, or phosphatidylinositol 3-kinase inhib itor wortmannin after SAH. Modified Garcia score, SAH grades, brain water content, Evans blue leakage, transmission electron microscope, immunohistochemistry...
Source: Molecular Neurobiology - February 25, 2017 Category: Neurology Source Type: research
MEKK1 Associated with Neuronal Apoptosis Following Intracerebral Hemorrhage.
In this study, we identified a MAPK kinase kinase (MAPKKK), MEKK1, may be involved in neuronal apoptosis in the processes of ICH through the activation of JNKs. From the results of western blot, immunohistochemistry and immunofluorescence, we obtained a significant up-regulation of MEKK1 in neurons adjacent to the hematoma following ICH. Increasing MEKK1 level was found to be accompanied with the up-regulation of p-JNK 3, p53, and c-jun. Besides, MEKK1 co-localized well with p-JNK in neurons, indicating its potential role in neuronal apoptosis. What's more, our in vitro study, using MEKK1 siRNA interference in PC12 cells, ...
Source: Neurochemical Research - September 22, 2016 Category: Neuroscience Authors: Lu H, Ning X, Tao X, Ren J, Song X, Tao W, Zhu L, Han L, Tao T, Yang J Tags: Neurochem Res Source Type: research
Pivotal Role of Brain Derived Neurotrophic Factor Secreted by Mesenchymal Stem Cells in Severe Intraventricular Hemorrhage in the Newborn Rats.
This study aimed to identify the paracrine mediator(s), and to determine their role in mediating the therapeutic effects of MSCs in severe IVH. We first identified significant up-regulation of brain-derived neurotrophic factor (BDNF) in MSCs compared with fibroblasts, in both DNA and antibody microarrays, after thrombin exposure. We then knocked down BDNF in MSCs by transfection with small interfering (si)RNA specific for human BDNF. The therapeutic effects of MSCs with or without BDNF knockdown were evaluated in vitro in rat neuronal cells challenged with thrombin, and in vivo in newborn Sprague-Dawley rats by injecting 2...
Source: Cell Transplantation - August 15, 2016 Category: Cytology Authors: Ahn SY, Chang YS, Sung DK, Sung SI, Ahn JY, Park WS Tags: Cell Transplant Source Type: research
Foxo1-mediated inflammatory response after cerebral hemorrhage in rats
In conclusion, our findings demonstrate that Foxo1 is a key regulator of inflammatory injury in rats after ICH. By identifying the molecular mechanisms of Foxo1/TLR4/NF-κB signaling, we provide a novel rationale for therapeutic approaches to managing inflammatory injury after ICH.
Source: Neuroscience Letters - July 16, 2016 Category: Neuroscience Source Type: research
Role of PDGF-D and PDGFR-β in neuroinflammation in experimental ICH mice model.
CONCLUSION: ICH-induced PDGF-D accumulation contributed to post-ICH inflammation via PDGFR activation and enhanced macrophage infiltration. The inhibition of PDGFR had an anti-inflammatory effect. Plasmin is a possible upstream effector of PDGF-D. The targeting of PDGF-D may provide a novel way to decrease brain injury after ICH.
PMID: 27302678 [PubMed - as supplied by publisher]
Source: Experimental Neurology - June 10, 2016 Category: Neurology Authors: Yang P, Manaenko A, Xu F, Miao L, Wang G, Hu X, Guo ZN, Hu Q, Hartman RE, Pearce WJ, Obenaus A, Zhang JH, Chen G, Tang J Tags: Exp Neurol Source Type: research
Role of hepcidin and its downstream proteins in early brain injury after experimental subarachnoid hemorrhage in rats.
In conclusion, downregulation of ferroportin-1 and ceruloplasmin caused by hepcidin enhanced iron-dependent oxidative damage and may be the potential mechanism of SAH.
PMID: 27250827 [PubMed - as supplied by publisher]
Source: Molecular and Cellular Biochemistry - May 31, 2016 Category: Biochemistry Authors: Tan G, Liu L, He Z, Sun J, Xing W, Sun X Tags: Mol Cell Biochem Source Type: research
Silencing of ataxia-telangiectasia mutated by siRNA enhances the in vitro and in vivo radiosensitivity of glioma.
In conclusion, silencing of ATM via the siRNA technique could improve the in vitro and in vivo radiosensitivity of glioma cells.
PMID: 27108486 [PubMed - as supplied by publisher]
Source: Oncology Reports - April 27, 2016 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research
Tozasertib attenuates neuronal apoptosis via DLK/JIP3/MA2K7/JNK pathway in early brain injury after SAH in rats.
CONCLUSIONS: Tozasertib reduced neuronal apoptosis and improved outcome possibly via DLK/JIP3/MA2K7/JNK pathways after SAH.
PMID: 27084696 [PubMed - as supplied by publisher]
Source: Neuropharmacology - April 11, 2016 Category: Drugs & Pharmacology Authors: Yin C, Huang GF, Sun XC, Guo Z, Zhang JH Tags: Neuropharmacology Source Type: research
