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Matrix Metalloproteinase-9 Expression is Enhanced by Ischemia and Tissue Plasminogen Activator and Induces Hemorrhage, Disability and Mortality in Experimental Stroke
Publication date: Available online 17 January 2021Source: NeuroscienceAuthor(s): Sofiyan Saleem, Dong Wang, Tieqiang Zhao, Ryan D. Sullivan, Guy L. Reed
Source: Neuroscience - January 18, 2021 Category: Neuroscience Source Type: research

Levetiracetam, an antiepileptic drug has neuroprotective effects on intracranial hemorrhage injury
Publication date: Available online 11 February 2020Source: NeuroscienceAuthor(s): Takahiko Imai, Tomoki Sugiyama, Sena Iwata, Shinsuke Nakamura, Masamitsu Shimazawa, Hideaki HaraAbstractIntracranial hemorrhage (ICH) is a devastating disease that induces hematoma formation with poor neuronal outcome. Levetiracetam (LEV) has been approval for epilepsy seizures. In a previous study, LEV exerted protective effects on cerebral ischemia models; however, the detail effects and the influence of LEV on ICH are still unknown. The aim of this study was to investigate whether oral administration of LEV (50 or 150 mg/kg) has protective...
Source: Neuroscience - February 13, 2020 Category: Neuroscience Source Type: research

Cattle Encephalon Glycoside and Ignotin Reduce Early Brain Injury and Cognitive Dysfunction after Subarachnoid Hemorrhage in Rats
This study explores a potential treatment for cognitive dysfunction following SAH with the demonstration that multi-target drug cattle encephlon glycoside and ignotin (CEGI) can relieve cognitive dysfunction by decreasing hippocampal neuron apoptosis following SAH in rats. Experimentally, 110 male SD rats were separated at random into Sham (20), SAH+Vehicle (30), SAH+4ml/kg CEGI (30), and SAH+1ml/kg CEGI groups (30) and an endovascular perforation model was created to induce SAH. We discovered that the number of TUNEL positive neurons in the hippocampus was markedly decreased in SAH+4ml/kg and SAH+1ml/kg CEGI groups compar...
Source: Neuroscience - July 21, 2018 Category: Neuroscience Source Type: research

Matrix Metalloproteinase-9 Mediates the Deleterious Effects of α2-Antiplasmin on Blood–Brain Barrier Breakdown and Ischemic Brain Injury in Experimental Stroke
We examined the hypothesis that MMP-9 is an essential downstream mediator of α2-antiplasmin’s deleterious effects during brain ischemia. Middle cerebral artery thromboembolic stroke was induced in a randomized, blinded fashion in mice with increased blood levels of α2-antiplasmin. There was a robust increase in MMP-9 expression (immunofluorescence) in the ischemic vs. the non-ischemic hemisphere of MMP-9+/+ but not MMP-9−/− mice, 24 h after stroke. Brain swelling and hemorrhage were significantly increased in the ischemic vs. the non-ischemic hemisphere of MMP-9+/+ mice. By comparison to MMP-9+/+ mice, the ischem...
Source: Neuroscience - March 3, 2018 Category: Neuroscience Source Type: research

Gabapentin prevents cortical spreading depolarization-induced disinhibition
Publication date: 11 October 2017 Source:Neuroscience, Volume 361 Author(s): Masoud Mesgari, Johanna Krüger, Christopher Theo Riemer, Maryam Khaleghi Ghadiri, Stjepana Kovac, Ali Gorji Cortical spreading depolarization (CSD) has an important role in brain diseases such as stroke, subarachnoid hemorrhage, migraine with aura, and epilepsy. Several anti-epileptic drugs (AEDs) are used to treat paroxysmal brain diseases and are thus known to suppress CSD. One of these AEDs is gabapentin (GBP) which has been traditionally used for treatment of some CSD-related neurological diseases. We applied intra- and extracellular recordi...
Source: Neuroscience - September 2, 2017 Category: Neuroscience Source Type: research

Role of thrombin-PAR1-PKC θ/δ axis in brain pericytes in thrombin-induced MMP-9 production and blood–brain barrier dysfunction in vitro
Publication date: 14 May 2017 Source:Neuroscience, Volume 350 Author(s): Takashi Machida, Shinya Dohgu, Fuyuko Takata, Junichi Matsumoto, Ikuya Kimura, Mariko Koga, Keiko Nakamoto, Atsushi Yamauchi, Yasufumi Kataoka Thrombin, an essential component in the coagulation cascade, participates in the pathogenesis of brain diseases, such as ischemic stroke, intracerebral hemorrhage, Alzheimer’s disease and Parkinson’s disease through blood–brain barrier (BBB) dysfunction. It is thought that the thrombin-matrix metalloproteinase (MMP)-9 axis is an important process in the pathogenesis of neurovascular disease, such as BBB ...
Source: Neuroscience - April 10, 2017 Category: Neuroscience Source Type: research

The role of connexin43 in hemorrhagic transformation after thrombolysis in vivo and in vitro
We examined whether the effects were Cx43 dependent using multiple Cx43 inhibitors. Phosphorylated Cx43 (p-Cx43) but not total Cx43 protein expression was increased after rtPA treatment. Delayed rtPA administration induced significant HT and BBB disruption. These effects were attenuated by inhibitors that blocked GJIC and Cx43 phosphorylation and expression but not Cx43 redistribution. Additionally, rtPA administration upregulated p-Cx43 expression in hypoxia/reoxygenation (H/R)-exposed brain endothelial cells. These effects were suppressed by the phosphatidylinositol 3′-kinase (PI3K) inhibitor LY294002 and the extracell...
Source: Neuroscience - May 18, 2016 Category: Neuroscience Source Type: research

Peroxynitrite decomposition catalyst prevents matrix metalloproteinase-9 activation and neurovascular injury after hemoglobin injection into the caudate nucleus of rats
Publication date: 25 June 2015 Source:Neuroscience, Volume 297 Author(s): R. Ding , L. Feng , L. He , Y. Chen , P. Wen , Z. Fu , C. Lin , S. Yang , X. Deng , J. Zeng , G. Sun Hemoglobin (Hb) is a major constituent of blood and a potent mediator of oxidative or nitrative stress after intracerebral hemorrhage (ICH). Our previous study demonstrated that Hb could induce abundant peroxynitrite (ONOO−) formation in vivo, which may be involved in the blood–brain barrier (BBB) disruption, however, the drug intervention is absent and also the underlying mechanism. Using an experimental stroke model by injecting Hb into the ca...
Source: Neuroscience - April 20, 2015 Category: Neuroscience Source Type: research

HMGB1 may act via RAGE to promote angiogenesis in the later phase after intracerebral hemorrhage
Publication date: 4 June 2015 Source:Neuroscience, Volume 295 Author(s): C. Lei , S. Zhang , T. Cao , W. Tao , M. Liu , B. Wu Following intracerebral hemorrhage (ICH), high-mobility group box 1 protein (HMGB1) may promote vascular remodeling. Whether HMGB1 supports angiogenesis after ICH is unclear, as are the receptors and downstream signaling pathway(s) involved. We used the rat model of collagenase-induced ICH to determine whether HMGB1 acts via the receptor for advanced glycation end-products (RAGE) to upregulate vascular endothelial growth factor (VEGF), a potent mitogen of endothelial cells and key regulator of nor...
Source: Neuroscience - April 6, 2015 Category: Neuroscience Source Type: research