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Condition: Epilepsy

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Total 35 results found since Jan 2013.

Effects of Brain IKKβ Gene Silencing by Small Interfering RNA on P-Glycoprotein Expression and Brain Damage in the Rat Kainic Acid-Induced Seizure Model.
Abstract Multidrug resistance mediated by over-expression of P-glycoprotein (P-gp) in brain is an important mechanism accounting for the drug-therapy failure in epilepsy. Over-expression of P-gp in epilepsy rat brain may be regulated by inflammation and nuclear factor-kappa B (NF-κB) activation. Inhibitory κB kinase subunit β (IKKβ) is an up-stream molecular controlling NF-κB activation. With the small interfering RNA (siRNA) technique and kainic acid (KA)-induced rat epileptic seizure model, the present study was aimed to further evaluate the role of NF-κB inhibition, via blocking IKKβ gene transcription, ...
Source: CNS and Neurological Disorders Drug Targets - August 27, 2013 Category: Drugs & Pharmacology Authors: Yu N, Liu H, Zhang YF, Su LY, Liu XH, Li LC, Hao JB, Huang XJ, Di Q Tags: CNS Neurol Disord Drug Targets Source Type: research

HMGB1 regulates P-glycoprotein expression in status epilepticus rat brains via the RAGE/NF- κB signaling pathway.
HMGB1 regulates P-glycoprotein expression in status epilepticus rat brains via the RAGE/NF-κB signaling pathway. Mol Med Rep. 2017 Jun 14;: Authors: Xie Y, Yu N, Chen Y, Zhang K, Ma HY, Di Q Abstract Overexpression of P-glycoprotein (P-gp) in the brain is an important mechanism involved in drug‑resistant epilepsy (DRE). High-mobility group box 1 (HMGB1), an inflammatory cytokine, significantly increases following seizures and may be involved in upregulation of P‑gp. However, the underlying mechanisms remain elusive. The aim of the present study was to evaluate the role of HMGB1 and its downstream ...
Source: Molecular Medicine Reports - June 21, 2017 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Downregulation of microRNA-200c-3p reduces damage of hippocampal neurons in epileptic rats by upregulating expression of RECK and inactivating the AKT signaling pathway
ConclusionOur study provides evidence that downregulation of miR-200c-3p reduces damage of hippocampal neurons in epileptic rats by upregulating RECK and inactivating the AKT signaling pathway.Graphical abstract
Source: Chemico Biological Interactions - April 22, 2019 Category: Biochemistry Source Type: research

Downregulation of microRNA-200c-3p reduces damage of hippocampal neurons in epileptic rats by upregulating expression of RECK and inactivating the AKT signaling pathway.
CONCLUSION: Our study provides evidence that downregulation of miR-200c-3p reduces damage of hippocampal neurons in epileptic rats by upregulating RECK and inactivating the AKT signaling pathway. PMID: 31018114 [PubMed - indexed for MEDLINE]
Source: Chemico-Biological Interactions - June 28, 2019 Category: Molecular Biology Authors: Du Y, Chi X, An W Tags: Chem Biol Interact Source Type: research

Involvement of hypoxia-inducible factor-1 alpha in the upregulation of P-glycoprotein in refractory epilepsy
To explore the involvement of hypoxia-inducible factor-1 alpha (HIF-1α) in the upregulation of P-glycoprotein (P-gp) in refractory epilepsy. Brain tissue specimens were collected and analyzed for expression of HIF-1α and P-gp using an immunohistochemical (IHC) staining method in both refractory epilepsy group and control group. Correlation between HIF-1α and P-gp expression level in refractory epilepsy group was analyzed. Then, a hypoxia cell model was established by simulating the nerve cell hypoxic microenvironment in the human U251 cell line using cobalt chloride (CoCl2). Western blot analysis was used to detect expr...
Source: NeuroReport - November 6, 2019 Category: Neurology Tags: Cellular, Molecular and Developmental Neuroscience Source Type: research

Inhibition of Transient Receptor Potential Vanilloid 4 (TRPV4) Mitigates Seizures
The objective of this study was to investigate the role of transient receptor potential vanilloid 4 (TRPV4) in 4-aminopyridine (4-AP)-induced seizures and the underlying mechanism. We also provide evidence for the role of Yes-associated protein (YAP) in seizures. 4-AP was administered to mice or primary cultured astrocytes. YAP-specific small interfering RNA (siRNA) was administered to primary cultured astrocytes. Mouse brain tissue and surgical specimens from epileptic patient brains were examined, and the results showed that TRPV4 was upregulated, while astrocytes were activated and polarized to the A1 phenotype. The lev...
Source: Neurotherapeutics - February 18, 2022 Category: Neurology Source Type: research

Focal Scn1a knockdown induces cognitive impairment without seizures.
Abstract Cognitive impairment is a common comorbidity in pediatric epilepsy that can severely affect quality of life. In many cases, antiepileptic treatments fail to improve cognition. Therefore, a fundamental question is whether underlying brain abnormalities may contribute to cognitive impairment through mechanisms independent of seizures. Here, we examined the possible effects on cognition of Na(v)1.1 down-regulation, a sodium channel principally involved in Dravet syndrome but also implicated in other cognitive disorders, including autism and Alzheimer's disease. Using an siRNA approach to knockdown Na(v)1.1 s...
Source: Neurobiology of Disease - January 11, 2013 Category: Neurology Authors: Bender AC, Natola H, Holmes GL, Scott RC, Lenck-Santini PP Tags: Neurobiol Dis Source Type: research

Transport of gabapentin by LAT1 (SLC7A5).
Abstract Gabapentin is used in the treatment of epilepsy and neuropathic pain. Gabapentin has high and saturable permeability across the BBB, but no mechanistic studies underpinning this process have been reported. The aim of the current study was to investigate the transport of gabapentin in a model of the BBB, identify the important drug transporter(s) and to use mathematical modelling to quantify the processes involved. A human brain endothelial cell line (hCMEC/D3) was utilised as an in-vitro model of the BBB. Uptake of radiolabeled gabapentin into cells in the presence of chemical inhibitors, siRNA or overexp...
Source: Biochemical Pharmacology - May 25, 2013 Category: Drugs & Pharmacology Authors: Dickens D, Webb SD, Antonyuk S, Giannoudis A, Owen A, Rädisch S, Hasnain SS, Pirmohamed M Tags: Biochem Pharmacol Source Type: research

Studies for normal function of prion protein using knockout mice under the immunological or pathophysiological stress
ABSTRACT Deletion of cellular isoform of prion protein (PrPC) increased neuronal predisposition to damage by modulating to apoptosis, and the negative consequences to oxidative stress. In vivo studies demonstrated that PrPC‐deficient mice were more prone to seizure, depression and epilepsy induction, and exhibited an extent of the cerebral damage following an ischemic challenge or viral infection. Besides, adenovirus‐mediated PrPC over‐expression reduces brain damage in rat model of cerebral ischemia. In experimental autoimmune encephalomyelitis (EAE) PrPC‐deficient mice demonstrated more aggressive disease onset a...
Source: Microbiology and Immunology - May 1, 2014 Category: Microbiology Authors: Takashi Onodera, Akikazu Sakudo, Hirokazu Tsubone, Shigeyoshi Itohara Tags: Review Source Type: research

Review of studies that have used knockout mice to assess normal function of prion protein under immunological or pathophysiological stress
Abstract Deletion of cellular isoform of prion protein (PrPC) increases neuronal predisposition to damage by modulating apoptosis and the negative consequences of oxidative stress. In vivo studies have demonstrated that PrPC‐deficient mice are more prone to seizure, depression, and induction of epilepsy and experience extensive cerebral damage following ischemic challenge or viral infection. In addition, adenovirus‐mediated overexpression of PrPC reduces brain damage in rat models of cerebral ischemia. In experimental autoimmune encephalomyelitis, PrPC‐deficient mice reportedly have a more aggressive disease onset an...
Source: Microbiology and Immunology - July 8, 2014 Category: Microbiology Authors: Takashi Onodera, Akikazu Sakudo, Hirokazu Tsubone, Shigeyoshi Itohara Tags: Review Source Type: research

Inactivation of histone deacetylase 1 (hdac1) but not hdac2 is required for the glucocorticoid-dependent ccaat/enhancer binding protein α (c/ebpα) expression and preadipocyte differentiation.
In this study, we sought to demonstrate using two different strategies the definite role of HDACl in adipogenesis. By using siRNA-mediated knockdown of HDAC1 and by generating an enzymatically inactive HDAC1D181A by site-directed mutagenesis, we were able to show that HDAC1, but not HDAC2, suppresses GR-potentiated preadipocyte differentiation by decreasing C/ebpα and Pparγ expression levels at the onset of differentiation. Finally, we demonstrate that HDAC1D181A acts as a dominant negative mutant of HDACl during adipogenesis by modulating C/EBPβ transcriptional activity on the C/ebpα promoter. PMID: 25203139 [Pub...
Source: Endocrinology - September 9, 2014 Category: Endocrinology Authors: Kuzmochka C, Abdou HS, Haché RJ, Atlas E Tags: Endocrinology Source Type: research

Association of Alpha-Soluble NSF Attachment Protein with Epileptic Seizure
This study aimed to assess αSNAP expression in temporal lobe epilepsy (TLE) patients and pilocarpine-induced rat model and to determine whether altered αSNAP expression leads to increased susceptibility to seizures. The expression of αSNAP was assessed in the temporal lobe from patients with TLE and pilocarpine-induced epileptic rats. In addition, αSNAP expression was silenced by lentivirus pLKD-CMV-GFP-U6-NAPA (primer: GGAAGCATGCGAGATCTATGC) in animals. At day 7, the animals were kindled by pilocarpine and then the time of latency to seizure and the incidence of chronic idiopathic epilepsy seizures were assessed. The ...
Source: Journal of Molecular Neuroscience - July 8, 2015 Category: Neuroscience Source Type: research

Valproic acid protects against haemorrhagic shock‐induced signalling changes via PPARγ activation in an in vitro model
CONCLUSION AND IMPLICATIONSChanges in GSK3β‐Ser9 phosphorylation in in vivo haemorrhagic shock models can be modelled in vitro, and this has identified a role for PPARγ activation in the protective role of VPA.
Source: British Journal of Pharmacology - September 1, 2015 Category: Drugs & Pharmacology Authors: Alexandra M E Zuckermann, Roberto M La Ragione, Deborah L Baines, Robin S B Williams Tags: RESEARCH PAPER Source Type: research

FAM222B Is Not a Likely Novel Candidate Gene for Cerebral Cavernous Malformations
Cerebral cavernous malformations (CCMs) are prevalent slow-flow vascular lesions which harbour the risk to develop intracranial haemorrhages, focal neurological deficits, and epileptic seizures. Autosomal dominantly inherited CCMs were found to be associated with heterozygous inactivating mutations in 3 genes, CCM1(KRIT1), CCM2(MGC4607), and CCM3(PDCD10) in 1999, 2003 and 2005, respectively. Despite the availability of high-throughput sequencing techniques, no further CCM gene has been published since. Here, we report on the identification of an autosomal dominantly inherited frameshift mutation in a gene of thus far unkno...
Source: Molecular Syndromology - June 17, 2016 Category: Molecular Biology Source Type: research