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S100A9 protein activates microglia and stimulates phagocytosis, resulting in synaptic and neuronal loss.
Neurobiol Dis
January 2025
Neuroscience Institute, Lithuanian University of Health Sciences, LT-50161 Kaunas, Lithuania. Electronic address:
S100 calcium-binding protein A9 (S100A9, also known as calgranulin B) is expressed and secreted by myeloid cells under inflammatory conditions, and S100A9 can amplify inflammation. There is a large increase in S100A9 expression in the brains of patients with neurodegenerative diseases, such as Alzheimer's disease, and S100A9 has been suggested to contribute to neurodegeneration, but the mechanisms are unclear. Here we investigated the effects of extracellular recombinant S100A9 protein on microglia, neurons and synapses in primary rat brain neuronal-glial cell cultures.
View Article and Find Full Text PDFExploring the therapeutic potential of α-(Phenylselanyl) acetophenone in tumor necrosis Factor-α-Induced depressive-like and hyperalgesic behavior in mice.
Brain Res
January 2025
Programa de Pós-Graduação em Bioquímica e Bioprospecção (PPGBBio), Grupo de Pesquisa em Neurobiotecnologia - GPN, Universidade Federal de Pelotas, UFPel, Postal Code 96010-900, Pelotas, RS, Brazil; Programa de Pós-Graduação em Biotecnologia (PPGB), Grupo de Pesquisa em Neurobiotecnologia- GPN, Biotecnologia/Centro de Desenvolvimento Tecnológico, Universidade Federal de Pelotas, Pelotas, RS, Brazil. Electronic address:
Chronic pain and depression exhibit a high comorbidity, are challenging to manage, and their pathophysiology mechanisms are intricated and closely related to the up-regulation of pro-inflammatory response and oxidative stress. Chronic pain and depression often coexist and present significant management challenges. Their underlying pathophysiological mechanisms are complex and closely linked to the up-regulation of pro-inflammatory responses and oxidative stress.
View Article and Find Full Text PDFHydrogen Sulfide (HS) Generated in the Colon Induces Neuropathic Pain by Activating Spinal NMDA Receptors in a Rodent Model of Chronic Constriction Injury.
Neurochem Res
January 2025
Department of Orthopaedics, Tianjin Hospital, Tianjin University, Tianjin, China.
Neuropathic pain (NP) imposes a significant burden on individuals, manifesting as nociceptive anaphylaxis, hypersensitivity, and spontaneous pain. Previous studies have shown that traumatic stress in the nervous system can lead to excessive production of hydrogen sulfide (HS) in the gut. As a toxic gas, it can damage the nervous system through the gut-brain axis.
View Article and Find Full Text PDFλ-cyhalothrin induced sex-specific inflammation, glia activation and GABAergic interneuron disruption in the hippocampus of rats.
BMC Pharmacol Toxicol
January 2025
Department of Anatomy, College of Health Sciences, University of Ilorin, Ilorin, 240003, Nigeria.
Background: Glia mediated neuroinflammation and degeneration of inhibitory GABAergic interneurons are some of the hall marks of pyrethroid neurotoxicity. Here we investigated the sex specific responses of inflammatory cytokines, microglia, astrocyte and parvalbumin positive inhibitory GABAergic interneurons to λ-cyhalothrin (LCT) exposures in rats.
Methods: Equal numbers of male and female rats were given oral corn oil, 2 mg/kg.
Effects of Tasimelteon Treatment on Traumatic Brain Injury Through NRF-2/HO-1 and RIPK1/RIPK3/MLKL Pathways in Rats.
Mol Neurobiol
January 2025
Department of Pathology, Faculty of Veterinary Medicine, Burdur Mehmet Akif Ersoy University, Burdur, Turkey.
Secondary brain damageafter traumatic brain injury (TBI) involves oxidative stress, neuroinflammation, apoptosis, and necroptosis and can be reversed by understanding these molecular pathways. The objective of this study was to examine the impact of tasimelteon (Tasi) administration on brain injury through the nuclear factor erythroid 2-related factor 2 (NRF-2)/heme oxygenase-1 (HO-1) and receptor-interacting protein kinase 1 (RIPK1)/receptor-interacting protein kinase 3 (RIPK3)/mixed lineage kinase domain-like (MLKL) pathways in rats with TBI. Thirty-two male Wistar albino rats weighing 300-350 g were randomly divided into four groups: the control group, trauma group, Tasi-1 group (trauma + 1 mg/kg Tasi intraperitoneally), and Tasi-10 group (trauma + 10 mg/kg Tasi intraperitoneally).
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