Aims: Brain ischemia activates astrocytes in a process known as astrogliosis. Although this process has beneficial effects, excessive astrogliosis can impair neuronal recovery. Polyinosinic-polycytidylic acid (Poly IC) has shown neuroprotection against cerebral ischemia-reperfusion injury, but whether it regulates reactive astrogliosis and glial scar formation is not clear.
Methods: We exposed cultured astrocytes to oxygen-glucose deprivation/reoxygenation (OGD/R) and used a rat middle cerebral artery occlusion (MCAO)/reperfusion model to investigate the effects of Poly IC. Astrocyte proliferation and proliferation-related molecules were evaluated by immunostaining and Western blotting. Neurological deficit scores, infarct volumes and neuroplasticity were evaluated in rats after transient MCAO.
Results: In vitro, Poly IC inhibited astrocyte proliferation, upregulated Toll-like receptor 3 (TLR3) expression, upregulated interferon-β, and downregulated interleukin-6 production. These changes were blocked by a neutralizing antibody against TLR3, suggesting that Poly IC function is TLR3-dependent. Moreover, in the MCAO model, Poly IC attenuated reactive astrogliosis, reduced brain infarction volume, and improved neurological function. In addition, Poly IC prevented MCAO-induced reductions in soma size, dendrite length, and number of dendritic bifurcations in cortical neurons of the infarct penumbra.
Conclusions: By ameliorating astrogliosis-related damage, Poly IC is a potential therapeutic agent for attenuating neuronal damage and promoting recovery after brain ischemia.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4638223 | PMC |
| http://dx.doi.org/10.1111/cns.12469 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Colistin treatment causes neuronal loss and cognitive impairment via ros accumulation and neuronal plasticity alterations.
Biomed Pharmacother
January 2025
Departament de Farmacologia, Toxicologia i Química Terapèutica, Facultat de Farmàcia i Ciències de l'Alimentació, Universitat de Barcelona (UB), Av. de Joan XXIII, 27-31, Barcelona 08028, Spain; Institut de Neurociències, Universitat de Barcelona (UB), Passeig de la Vall d'Hebron, 171, Barcelona 08035, Spain; Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Instituto de Carlos III, Av. Monforte de Lemos, 3-5, Madrid 28029, Spain; Institut d'Investigació Sanitària Pere Virgili (IISPV), Hospital Universitari Sant Joan de Reus, Av. Josep Laporte, 2, Reus 43204, Spain. Electronic address:
The rise of antimicrobial resistance has made necessary the increase of the antibacterial arsenal against multidrug-resistant bacteria. In this context, colistin has re-emerged as a first-line antibiotic in critical situations despite its nephro- and neuro- toxicity at peripheral level. However, the mechanism underlying its toxicity remains unknown, particularly in relation to the central nervous system (CNS).
View Article and Find Full Text PDFDose-Dependent Effect of a New Biotin Compound in Hippocampal Remyelination in Rats.
Mol Neurobiol
January 2025
Department of Nutrition, Faculty of Veterinary Medicine, Firat University, Elazig, Turkey.
Demyelination is commonly observed in neurodegenerative disorders, including multiple sclerosis (MS). Biotin supplementation is known to stabilize MS progression. To reduce the effective dose of biotin, we synthesized a new and superior form of biotin, a complex of magnesium ionically bound to biotin (MgB) and compared its dose-dependent effect with biotin alone after inducing demyelination using lysolecithin (LPC) in rats.
View Article and Find Full Text PDFIntroduction: CLN8-Batten disease is a rare neurodegenerative disorder characterized phenotypically by progressive deterioration of motor and cognitive abilities, visual symptoms, epileptic seizures, and premature death. Mutations in CLN8 result in characteristic Batten disease symptoms and brain-wide pathology including accumulation of lysosomal storage material, gliosis, and neurodegeneration. Recent investigations of other subtypes of Batten disease (CLN1, CLN3, CLN6) have emphasized the influence of biological sex on disease and treatment outcomes; however, little is known about sex differences in the CLN8 subtype.
View Article and Find Full Text PDFRespiratory failure as main presentation sign of MAPT-related disorder.
J Neurol
January 2025
Centre de Génétique Humaine, Centre Hospitalier Universitaire de Besançon, Besançon, France.
Introduction: The MAPT gene encodes Tau, a protein mainly expressed by neurons. Tau protein plays an important role in cerebral microtubule polymerization and stabilization, in axonal transport and synaptic plasticity. Heterozygous pathogenic variation in MAPT are involved in a spectrum of autosomal dominant neurodegenerative diseases known as taupathies, including Alzheimer's disease, Pick's disease, fronto-temporal dementia, cortico-basal degeneration and progressive supranuclear palsy.
View Article and Find Full Text PDFRegulation of MAP2, GFAP, and calcium in the CA3 Region Following Kainic Acid Exposure to organotypic hippocampal slice culture.
F1000Res
January 2025
Faculty of Teaching and Education Sciences, Islamic University of Malang, Malang, East Java, Indonesia.
Background: Neurodegeneration due to neurotoxicity is one of the phenomena in temporal lobe epilepsy. Experimentally, hippocampal excitotoxicity process can occur due to kainic acid exposure, especially in the CA3 area. Neuronal death, astrocyte reactivity and increased calcium also occur in hippocampal excitotoxicity, but few studies have investigated immediate effect after kainic acid exposure.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!