In comparison to other stroke types, subarachnoid hemorrhage (SAH) is characterized by an early age of onset and often results in poor prognosis. The inadequate blood flow at the site of the lesion leads to localized oxygen deprivation, increased level of hypoxia-inducible factor-1α (HIF-1α), and triggers inflammatory responses and oxidative stress, ultimately causing hypoxic brain damage. Despite the potential benefits of oxygen (O) administration, there is currently a lack of efficient focal site O delivery following SAH. Conventional clinical O supply methods, such as transnasal oxygenation and hyperbaric oxygen therapy, do not show the ideal therapeutic effect in severe SAH patients. The perfluorocarbon oxygen carrier (PFOC) demonstrates efficacy in transporting O and responding to elevated levels of CO at the lesion site. Through cellular experiments, we determined that PFOC oxygenation serves as an effective therapeutic approach in inhibiting hypoxia. Furthermore, our animal experiments showed that PFOC oxygenation outperforms O breathing, leading to microglia phenotypic switching and the suppression of inflammatory response via the inhibition of HIF-1α. Therefore, as a new type of O therapy after SAH, PFOC oxygenation can effectively reduce hypoxic brain injury and improve neurological function.
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http://dx.doi.org/10.1016/j.freeradbiomed.2024.02.002 | DOI Listing |
Eur J Pediatr
January 2025
Neonatology Department. Hospital Sant Joan de Déu, Center for Maternal Fetal and Neonatal Medicine. Neonatal Brain Group, Universitat de Barcelona. Hospital Clínic, Universitat de Barcelona. BCNatal - Barcelona, Institut de Recerca Sant Joan de Déu, Barcelona, Spain.
Purpose: Perinatal hypoxic-ischemic encephalopathy (HIE) is a significant cause of neonatal brain injury. Therapeutic hypothermia (TH) is the standard treatment for term neonates, but its safety and efficacy in neonates < 36 weeks gestational age (GA) remains unclear. This case series aimed to evaluate the outcomes of preterm infants with HIE treated with TH.
View Article and Find Full Text PDFTheranostics
January 2025
Neurooncology Unit, Instituto de Investigación Biomédicas I+12, Hospital Universitario 12 de Octubre, Madrid 28041, Spain.
Glioblastoma IDH wild type (GBM IDH wt) has a poor prognosis and a strongly associated with inflammatory processes. Inflammatory molecules generate positive feedback with tumor cells fueling tumor growth as well as recruitment of immune cells that promote aggressiveness. Although the role of many inflammatory molecules is well known, there are many macromolecules, such as the S100A proteins, whose role is only now beginning to be established.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
Department of Neonatology and Pediatric Intensive Care, Children's Hospital University of Bonn, Bonn, Germany.
Neonatal hypoxic-ischemic encephalopathy (HIE) is the most common cause of death and long-term disabilities in term neonates. Caffeine exerts anti-inflammatory effects and has been used in neonatal intensive care units in recent decades. In our neonatal rat model of hypoxic-ischemic (HI) brain injury, we demonstrated that a single daily dose of caffeine (40 mg/kg) for 3 days post-HI reduced brain tissue loss and microgliosis compared to the vehicle group.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
Department of Otolaryngology Head and Neck Surgery/Deep Underground Space Medical Center, West China Hospital, Sichuan University, Chengdu, China.
Heat acclimation (HA) is an evolutionarily conserved trait that enhances tolerance to novel stressors by inducing heat shock proteins (HSPs). However, the molecular mechanisms underlying this phenomenon remain elusive. In this study, we established a HA mouse model through intermittent heat stimulation.
View Article and Find Full Text PDFCrit Rev Clin Lab Sci
January 2025
Institute of Metabolism and Systems Research (IMSR), University of Birmingham, Birmingham, West Midlands, UK.
We present a series of three articles on the genetics and pharmacogenetics of G protein- coupled receptors (GPCR). In the first article, we discuss genetic variants of the G protein subunits and accessory proteins that are associated with human phenotypes; in the second article, we build upon this to discuss "G protein-coupled receptor (GPCR) gene variants and human genetic disease" and in the third article, we survey "G protein-coupled receptor pharmacogenomics". In the present article, we review the processes of ligand binding, GPCR activation, inactivation, and receptor trafficking to the membrane in the context of human genetic disease resulting from pathogenic variants of accessory proteins and G proteins.
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